ALCOHOL USE

DISORDERS
BY CAROL NAKIMERA
JOHN FISHER BIRUNGI
S U P E RV I S O R : D R . I N E N A WA I N E N A
TOPIC OUTLINE
Introduction
Definitions
Epidemiology
Etiology
Risk factors and prognostics
Pathophysiology
Diagnosis
Alcohol intoxication
Alcohol withdrawal
Delirium tremens
Management
INTRODUCTION
Substance related and addictive disorders are symptomatic presentations that are
due to physiological effects of an exogenous substance on the central nervous
system.
Examples include;
1. Alcohol
2. Inhalants cocaine
3. Psychotropic medications (stimulants, sedative hypnotics)
4. Other medications e,g steroids
5. Environmental toxins e.g organophosphate insecticides
Introduction
Alcohol is a potent drug that causes both acute and chronic changes
in almost all neurochemical systems.

Thus alcohol abuse can produce severe, temporary psychological

symptoms including depression, anxiety, and psychosis.

Increasing levels of regular alcohol consumption can cause tolerance.

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DEFINITION
Alcohol use disorders
◦ Alcohol abuse + Alcohol dependence
Alcohol induced/related disorders
◦ Alcohol intoxication
◦ Alcohol withdrawal syndrome
◦ Alcohol hallucinosis
◦ Delirium Tremens
◦ Depression, Mania, Psychosis, Anxiety, Sleep, Sexual & Eating

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Definitions contd:
Alcohol use disorder is differentiated from alcohol intoxication ,
withdrawal, and alcohol induced mental disorders(e.g alcohol
induced depressive disorder ) in that alcohol use disorder describes a
problematic pattern of alcohol use that involves impaired control over
alcohol use, social impairment due to alcohol use, risky alcohol use
such as driving while intoxicated, and pharmacological symptoms
( the development of tolerance or withdrawal) whereas those above
describe psychiatric syndromes that develop in context of heavy use.
Defn cont’d,

Dependence. The term dependence is used in one of two ways. In behavioral

dependence, substance-seeking activities and related evidence of pathologic
use patterns are emphasized with or without physical dependence. Physical
dependence indicates an altered physiologic state due to repeated
administration of a drug, the cessation of which results in a specific syndrome
Abuse. Use of any drug, usually by self-administration, in a manner that
deviates from approved social or medical patterns.
Misuse. Similar to abuse but usually applies to drugs prescribed by physicians
that are not used properly.
Addiction. The repeated and increased use of a substance, the deprivation of
which gives rise to symptoms of distress and an irresistible urge to use the
agent again and which leads also to physical and mental deterioration. The
term is no longer included in the official nomenclature, having been replaced
by the term dependence, but it is a useful term in common usage.
Defn cont’d
Intoxication. A reversible syndrome caused by a specific substance that
effects one or more of the following mental functions: memory, orientation,
mood, judgment, and behavioral, social, or occupational functioning.
Withdrawal. A substance-specific syndrome that occurs after stopping or
reducing the amount of the drug or substance that has been used regularly over
a prolonged period of time. The syndrome is characterized by physiologic
signs and symptoms in addition to psychological changes such as disturbances
in thinking, feeling, and behavior. Also called abstinence syndrome or
discontinuation syndrome.
Tolerance. Phenomenon in which, after repeated administration, a given dose
of a drug produces a decreased effect or increasingly larger doses must be
administered to obtain the effect observed with the original dose. Behavioral
tolerance reflects the ability of the person to perform tasks despite the effects
of the drug.
Defn cont’d

Cross-tolerance. Refers to the ability of one drug to be substituted for

another, each usually producing the same physiologic and psychological
effect (e.g., diazepam and barbiturates). Also known as cross dependence.
Co-dependence. Term used to refer to family members affected by or
influencing the behavior of the substance abuser. Related to the term enabler,
which is a person who facilitates the abuser’s addictive behavior (e.g.,
providing drugs directly or money to buy drugs). Enabling also includes the
unwillingness of a family member to accept addiction as a medical–
psychiatric disorder or to deny that the person is abusing a substance.
Neuroadaptation. Neurochemical or neurophysiologic changes in the body
that result from the repeated administration of a drug. Neuroadaptation
accounts for the phenomenon of the metabolizing system in the body. Cellular
or pharmacodynamics adaptation refers to the ability of the nervous system to
function despite high blood levels of the offending substance.
EPIDEMIOLOGY
According to the alcoholism by country statistics (Our World in Data 2021), the
yearly average alcohol use worldwide is 6.4litres for individual older than 15
year old.
Globally , one in three people (32.5%) drink alcohol-equivalent to 2.4 billion
people – including 25% of women(0.9 billion women ) and 39% of men (1.5
billion men.) on average , each women consumed 0.73 alcoholic drinks and men
drank 1.7 drinks.
Currently, the Seychelles is in first place with around 20.5 litres of alcohol drunk
per person per year, according to Our World in Data.
Epidemiology
75% of Ugandans regularly engages in varying levels of alcohol
consumption. (~50% men, 25% women)
18-35 years account for 85% drinkers
60% exceed safe limits
Uganda top in Africa and 7th in world (2019 data) ~12.48 liters per
capita
epidemiology
Lifetime prevalence of alcohol dependence (United States)
◦ 3-5% of women and 10% of men
◦ Twice as many people meet diagnostic criteria for alcohol abuse during their
lifetimes
Most common co-ingestant in drug overdose
Commonest cause of Intellectual Disability in USA
◦ F.A.S(Foetal Alcohol Syndrome)
◦ Neural tube defects
there is a sevenfold risk of alcohol dependence in first-degree relatives of
alcohol-dependent individuals, especially among men.
◦ 76.4 million people worldwide suffered from an alcohol use disorder

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epidemiology
Alcohol consumption in the United States is greatest among young
men 18 to 25 years old; the prevalence of current drinking decreases
with increasing age

The lowest prevalence is seen among non-Hispanic Blacks and

Asians.

College-educated individuals are almost twice as likely to be current

drinkers as individuals with less than a high school education..

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ETIOLOGY
BIOPSYCHOSOCIAL MODEL
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RISK FACTORS AND PROGNOTICS
1. Environmental – poverty
- discrimination( structural inequities such as differential
incarceration rates, and differential access to medications for addiction treatment.)
- unemployment
- low levels of educations
-cultural attitudes towards drinking and intoxication
- availability of alcohol (price)
- stress levels
RISK FACTORS contd;
2. genetics and physiological : runs in families with 40-60% of the
variance of risk explained by genetics influences . The rate is 3 to 4
times higher in close relatives of individual with alcohol use
disorders.
PATHOPHYSIOLOGY
Metabolism

◦ Alcohol~ acetaldehyde (alcohol dehydrogenase)

◦ Acetaldehyde ~acetic acid (aldehyde dehydrogenase)
◦ MEOS (microsomal ethanol oxidizing system )
◦ CYP2E1
◦ Catalase
This first-pass metabolism appears to be important in determining alcohol
toxicity since its efficiency determines alcohol bioavailability.
92% to 95% of the alcohol that is ingested is metabolized in the liver by ADH.
90% to 95% of ingested alcohol is eliminated as water and CO2.

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Effects of Alcohol on Neurotransmission
Alcohol enhances dopamine release in ventral tegmental area
Alcohol administration also enhances GABAergic inhibitory effects
presynaptically by increasing GABA (γ-aminobutyric acid) release
Acute administration of alcohol antagonizes NMDA (N-Methyl-d-aspartate)
receptors
Alcohol administration stimulates hypothalamic synthesis, release, and binding
of endogenous opioids such as β-endorphin and enkephalin to μ-opiate
receptors
Pharmacologic manipulation of the nicotinic cholinergic receptor with
mecamylamine or varenicline appears to reduce the stimulant effects of acute
alcohol administration and alcohol consumption.
chronic exposure to alcohol reduces 5-HT concentrations in the brain, which is
associated with impulsive aggression and behavioral disinhibition
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GABA and serotonin receptor activation
Glutamate and voltage-gated calcium channels receptor inhibition
Thus, alcohol is a potent CNS depressant

Upregulation of enzymes in heavy drinkers

◦ Tolerance
Asians often have less aldehyde dehydrogenase (gene variant)
◦ Flushing and nausea and protecting against alcohol dependence.
Determinants of alcohol consumption
Greater absorption in jejunum and duodenum (80%) & stomach
(20%)

Severity associated with rapid ingestion

alcohol shows little solubility in fat

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History taking/clerkship
First – Worst – Last episode
◦ Onset
◦ Timing (frequency & duration)
◦ Amount, types
◦ Effects of intoxication/withdrawal
◦ 4P’s
◦ Consequences/Complications
◦ Other drugs (above 6 points apply)

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Evaluation
Detailed &systematic evaluation of alcohol-dependent patients
A complete drinking history should be obtained, including questions on
◦ typical quantity and frequency of alcohol consumption,
◦ maximal number of drinks per drinking occasion,
◦ frequency of heavy drinking episodes, history of alcohol-related problems,
◦ psychiatric symptoms and the nature of their relationship with alcohol
consumption (e.g., precipitation or exacerbation),
◦ history of medical complications.

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Natural history of alcohol intake
In the early phases of the disorder (early and mid- twenties), the most prominent
feature is daily heavy drinking or frequent binge drinking.
Individuals describe a rewarding sense of euphoria and elation that immediately
follows the first drinks.

As heavy drinking persists, tolerance to alcohol’s effects sets in

Increased frequency and intensity of drinking may be associated with irresistible
urges to drink or craving.

With time, the person experiences increasing days absent from work, frequent
family, conflicts, and other interpersonal and legal problems.
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ALCOHOL INTOXICATION
30
Management:BIOPSYCHOSOCIAL
MODEL
Investigations contd;
RBS
LFTS
RFTS
ELECTROLYTES
CT SCAN IN CASE OF HEAD TRAUMA
TOXICOLOGY:BLOOD ALCOHOL LEVEL/CONCENTRATION, ALCOHOL IN URINE
SCREENING
CAGE, which includes four questions:
◦ (1) Have you ever felt you ought to cut (the “C” in CAGE) down on your drinking?
◦ (2) Have people annoyed (A) you by criticizing your drinking?
◦ (3) Have you ever felt bad or guilty (G) about your drinking?
◦ (4) Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover,
that is, an eye-opener (E)?
◦ A total CAGE score of 2 or greater (at least 2 of the items are endorsed as being positive) is considered
highly suggestive of an alcohol use disorder.

Alcohol Use Disorders Identification Test (AUDIT), which consists of 10 items. The AUDIT is
sensitive and specific in the identification of hazardous or harmful drinkers, and can identify
alcohol-dependent individuals. The AUDIT’s cutoff score is 8 for detecting alcohol use
disorders.

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 TREAMENT:DETOXIFICATION
Monitor: ABC, GLUCOSE, electrolytes, acid-base status
Give THIAMINE 100mg IV/IM (to prevent or treat Wernicke's encephalopathy) and folate
Naloxone may be necessary to reverse effects of co-ingested opioids
Symptomatic Management
◦ Sleeping “it” off

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PSYCHOTHERAPY
1. Group therapy
2. Interpersonal therapy
3. Family therapy
4. Cognitive behavioral therapy
TREATMENT
The goal is the prolonged maintenance of total sobriety. Relapses are common.
Initial treatment requires detoxification and management of presenting symptoms.
Insight
Psychotherapy : group therapy(more effective than individual therapy) especially for patietns
who perceive alcohol dependence a societal rather than a personal psychiatric problem.
Alcoholics anonymous (AA for patients ) and AI-Anon( for families of patients).
Social: cognitive skills, social skills
LONG TERM MANAGEMENT
Disulfiram (Antiabuse.
Dose daily is 250 to 500mg of disulfiram .
Moa : inhibits acetaldehyde dehydrogenase hence resulting into accumulation gf acetaldehyde in
the liver.
Patients experience headaches, flushing, hypotension, sweating , anxiety, hyperventilation ,
tachycardia and other life threatening conditions in case of ingestion of even the smallest amounts
of alcohol.
Contraindications:
patients with heart disease
Cerebral thrombosis
Diabetes mellitus
NB: SHOLD BE USED TEMPORARILY TO ESTABLISH LONG TERM SOBRIETY

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Cont:
Naltrexone (Revia, IM Vivitrol)
It decreases a craving for alcohol probably by blocking the release of endogenous opioids hence aiding
the patient to achieve their goal.
Greater benefit is seen in persons with family history of alcoholism
In patients with physical opioid dependence, it will precipitate withdrawal
Dosage: 50mg once daily.

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 Cont:
Acamprosate ( Campral)
Structurally similar to GABA
Should be started post-detoxification for relapse prevention in patients who have stopped drinking
Major advantage is that it can be used in patients with liver disease
Contraindicated in severe renal disease

Topiramate (Topamax)
Anticonvulsant that potentiates GABA and inhibits glutamate receptors
Reduces cravings for alcohol

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FDA approved dosages:
Disulfiram 500 mg po od; Target dose 500 mg
Naltrexone 50 mg po od or 380 mg IM q monthly
Acamprosate 666 mg TID
Topiramate 25 mg BID x 1/52 then increasing over 8 weeks by 25 mg per week; Target dose
200 mg BID

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Stages of changes

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ALCOHOL WITHDRAWAL
Potentially lethal
Insomnia, anxiety, hand tremor, irritability, anorexia, nausea,
vomiting, autonomic hyperactivity (diaphoresis, tachycardia,
hypertension), psycho-motor agitation, fever, seizures,
hallucinations, and delirium
Earliest symptoms (6 - 24 hrs); depend on the duration and quantity
of alcohol consumption
◦ Symptomatic Management
◦ Abstinence vs Harm Reduction
seizures (6 - 48 hrs); peak around 13-24 hrs
◦ 1/3 with seizures develop delirium tremens
◦ Hypomagnesemia may predispose to seizures; correct promptly
◦ Treat with benzodiazepines, Phenytoin(Dilantin)

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Seizures associated with alcohol withdrawal are stereotyped, generalized, and tonic–clonic in
character

Seizure activity in patients with known alcohol abuse histories should still prompt clinicians to
consider other causative factors, such as head injuries, CNS infections, CNS neoplasms, and
other cerebrovascular diseases.

Long-term severe alcohol abuse can result in hypoglycemia, hyponatremia, and

hypomagnesemia—all of which can also be associated with seizures

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ALCOHOL WITHDRAWAL
DDx:
a) Other medical conditions such as diabetic acidosis and neurological conditions such as
cerebral ataxia, multiple sclerosis
b) Alcohol induced mental disorders such as alcohol induced depressive
c) Sedative , hypnotic or anxiolytic intoxication
DELIRIUM TREMENS
Most severe form of withdrawal
Begins 48 - 72 hrs
May occur later (90% of cases within 7 days)

5% of patients hospitalized for EtOH withdrawal

15-25% mortality rate if untreated

Risk factors; Physical illness, Male (4 – 5x)

Symptoms; delirium, hallucinations (most commonly visual), gross tremors, autonomic
instability, and fluctuating levels of psychomotor activity
Medical emergency and should be treated with adequate doses of benzodiazepines up to a
dose of 60mg/kg/BWT)

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DELIRIUM TREMENS
Monitor withdrawal signs and symptoms
Clinical Institute Withdrawal Assessment (CIWA)
Benzodiazepines (chlordiazepoxide, scale
diazepam, or lorazepam) sufficient doses
patient calm and lightly sedated, then tapered Careful attention; level of consciousness,
down slowly possibility of trauma
OR Carbamezepine or valproate taper can Check for signs of hepatic failure e.g. ascites,
be used jaundice, caput medusae, coagulopathy
Antipsychotics and temporary restraints for
severe agitation
Thiamine, folic acid, and a multivitamin for
nutritional deficiencies
Electrolyte and fluid abnormalities

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COMPLICATIONS
Medical
◦ Hypoglycemia, Dehydration, Alcohol Poisoning, Hangover Symptoms
◦ Metabolic acidosis
◦ Increased anion gap
◦ Methanol & ethylene glycol poisoning

Marital conflict & Work problems

◦ Child abuse & neglect
◦ Poverty, Poor job performance/Loss of employment
◦ Domestic violence
◦ High Expressed Emotions(Over involvement-Criticism-Hostility)
◦ Death

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COMPLICATIONS
Liver complications; HIV; Neurocognitive disorders; Malnutrition; CVDs; Addiction
Wernicke's encephalopathy
◦ Thiamine deficiency resulting from poor nutrition
◦ Acute and can be reversed with thiamine therapy
◦ Features: Ataxia (broad-based), confusion, ocular abnormalities (nystagmus, gaze palsies)
◦ If left untreated, Wernicke's encephalopathy may progress to Korsakoff syndrome

Korsakoff syndrome
◦ Chronic amnestic syndrome
◦ Reversible in only about 20% of patients
◦ Features: Impaired recent memory, anterograde amnesia, ‘compensatory’ confabulation

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MANAGEMENT
BioPsychoSocial model
Investigations
◦ C.A.G.E & AUDIT (screening)
◦ BAL
◦ LFTs
◦ AST : ALT ratio = or > 2 : 1

Elevated GGT, CDT (carbohydrate deficient Transferrin) and MCV (Erythrocyte mean
corpuscular volume)
The alcohol breath test measures the amount of alcohol in expired air, providing an estimate of
venous BAL.

◦ AUDIT (diagnosing)

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REFERENCES
KAPLAN & SADOCK POCKET HANDBOOK OF PSYCHIATRY 6th EDITION,substabce related and
addictive disorders, pg125
DSM-5 TR, substance related and addictive disorders pg753.