ALCOHOL- & DRUG-

RELATED PROBLEMS
(GROUP 7)
 PREPARED BY:
1. Nur Izz Sabrina binti Othman (78403)
2. Stephanie Bacha anak Menari (78549)
3. Reshme Ashwini A/P Rajasegar (81047)
4. Peter Wong Qin Chai (80955)
5. Muhammad Harith bin Noorddin (78246)

6. Nurul Akma Azma Azzahra binti Ramli (78459)

7. Marie Isabel anak Nanang (78129)
8. Airul Shamirzuan bin Mohamad Safri (77779)
 OUTLINE
1. Alcohol use disorder & alcohol-related disorder
2. Other substances

3. Substance-induced psychotic disorder

Alcohol Use Disorder
MECHANISM OF ACTION OF ALCOHOL
Wow!
Ethanol is a small molecule that is both lipid and water soluble.
Readily absorbed from the intestine by passive diffusion.
A small percentage of ingested ethanol (0% to 5%) enters the gastric
mucosal cells of the upper gastrointestinal (GI) tract (tongue, mouth,
esophagus, and stomach), where it is metabolized.
The remainder enters the blood.
Of this, 85% to 98% is metabolized in the liver, and only 2% to 10% is
excreted through the lungs or kidneys.
The major enzymes involved in metabolizing ethanol are alcohol
dehydrogenase, acetaldehyde dehydrogenase, and the microsomal ethanol
oxidizing system (MEOS).

Marks' Basic Medical Biochemistry. A Clinical Approach 5th Edition.

 DIFFERENT TYPES OF ALCOHOLIC
BEVERAGES AND PERCENTAGE (%)
Alcoholic beverages in stores
Bir (Beer, Stout); Low alcohol
Wain (Wain buah-buahan, wain beras); Moderate alcohol
Likuor dan spirit (Liquor, Gin, Rum, Vodka); High alcohol

Traditional alcoholic drinks / home made

Todi, Bahar. Ijok; Moderate alcohol
Tuak Beras, Air tapai, Lihing; Moderate alcohol
Montoku, Langkau, Samsu; High alcohol

GARIS PANDUAN SARINGAN DAN INTERVENSI PENCEGAHAN DAN PENGURANGAN KEMUDARATAN ALKOHOL 2013
Sample measurements for 1 traditional
alcoholic drink:
Bahar/ Ijok/ Todi : 4 hirup/ 120 ml = 1
standard drink
Air tapai/ Tuak beras/ Lihing : 3 hirup/
90 ml = 1 standard drink
Montoku/ Langkau/ Samsu : 1 hirup/
30 ml = 1 standard drink

GARIS PANDUAN SARINGAN DAN INTERVENSI PENCEGAHAN DAN PENGURANGAN KEMUDARATAN ALKOHOL 2013
 FORMULA TO CALCULATE ALCOHOL
CONSUMPTION (UNIT) - UK
Alcohol Consumption (Unit)
=strength (alcohol by volume or ABV) x the volume of the drink (in ml) ÷ 1,000

Example: 568ml beer with 4% alcohol content

Alcohol Consumption
= (4% x 568 ml) ÷ 1000
=2.3 Units

The alcohol units per week for both man and woman are equal, which is
14 units per week.

Alcohol Change UK - Alcohol Units ; Oxford of Psychiatry 4th Edition; UK Chief Medical Officers’ Low Risk Drinking Guidelines
 FORMULA TO CALCULATE ALCOHOL
CONSUMPTION (MALAYSIA)

GARIS PANDUAN SARINGAN DAN INTERVENSI PENCEGAHAN DAN PENGURANGAN KEMUDARATAN ALKOHOL 2013
 FORMULA TO CALCULATE ALCOHOL
CONSUMPTION (MALAYSIA)

Example: 100ml wine with 12% alcohol content

Standard Drink Equivalent
= [ 100ml x (12%÷100%) x 0.79 alcohol/ml ] ÷ 10 grams
=0.95 Standard drink

A standard drink is equal to 10 grams of pure alcohol.

GARIS PANDUAN SARINGAN DAN INTERVENSI PENCEGAHAN DAN PENGURANGAN KEMUDARATAN ALKOHOL 2013
 Complication of alcohol misuse
Give me a
Neurological complication
break. Peripheral
- Neuropsychiatric phenomena
- Peripheral neuropathy
- Cognition
Sexual dysfunction
Wernicke’s encephalopathy
- Sexual dysfunction
- Ataxia, ophthalmophlegia, memory disturbances
Lower GIT
- Severe: Korsakoff psychosis
- Gastritis
Alcoholic hallucinosis
Heart
Seizure
- Coronary artery disease
Liver
- Cardiomyopathy
- Liver function impairment
- Heart failure
Upper GIT
- Arrhythmia
- Cancer of mouth, pharynx, and esophagus
Effect of alcohol on women Fetal alcohol syndrome
Prone to have gynecological Facial abnormality
complications: Small stature
Low birth-weight
- amenorrhea Low intelligence
- anovulation
- early menopause
Increase risk of having breast
cancer
Pregnant lady ---> fetal alcohol
syndrome
Fetal Alcohol Syndrome
 Social damage
Family problem
- Marital and family tension
- Violence
- Depressed spouse
- Poor role model
- Emotional and behavioral problem in children
Work difficulties
- Poor performance
- Unemployment
Crime
- Sexual offense
- Murder
Assessment of patient with alcohol
abuse / dependence
1. History
2. Mental State Examination (MSE)
3. Physical examination
1. History
Describe a typical day’s drinking. What time is first drink of the day?
When did daily drinking start?
Period of abstinence (if any), what factor helped to maintain?
What led to a resumption of drinking?
Presence of withdrawal symptoms in morning / after abstinence
Previous attempt at treatment
Any medical complication (e.g. gastritis, liver damage, etc)
Patient’s attitude towards drinking
 2. Mental State Examination (MSE)
Appearance and behavior:
o General appearance, grooming, etc. Caution regarding cultural norms. E.g. ‘grunge’ look is appropriate for some youth culture
o Slow or accelerated movements, anxious looking behavior
Speech:
o Note volume and rate of speech, e.g. pressure of speech might indicate amphetamine use or mania
Mood and affect:
o Mood refers to the sustained emotional tone as reported by the individual, e.g. depressed, angry, irritable, or anxious
o Affect refers to the varying emotional response witnessed during the interview, e.g. appropriate, flat, labile, fatuous.

Perception:
o Experiencing hallucinations in any sensory area (visual, gustatory, olfactory, auditory), e.g. alcoholic hallucinosis tend to feel
things crawling over their skin and have illusion
Thought:
o Thought disorders – thought process and thought content
Cognition:
o Orientation (time/place/person), attention and concentration, memory (immediate/recent/remote), information and intelligence,
abstract thinking

Insight:
o Patient’s awareness and understanding of illness and need for treatment
Judgement:
o Patient’s understanding of the likely outcome of behavior, and whether that understanding influences the behavior
3. Physical examination
- Blood pressure
- CVS examination
- CNS examination
- Abdominal examination (enlarged liver, spider naevi, jaundice)
Investigations
1. Biological
Blood alcohol concentration (BAC)
Gamma glutamyl transferase (GGT)
Mean corpuscular volume (MCV)
Carbohydrate deficient transferrin (CDT)

2. Psychological
Questionnaire-based assessments (AUDIT & CAGE)
Blood Alcohol Concentration (BAC)
Measures recent alcohol consumption
Unit: mg of alcohol per 100mL of blood (mg%)
Correlates well with breath alcohol measured by breathalyser
Useful in assessing recent drinking and as an objective measure of intoxication (in
Emergency Department)
Discrepancy between high BAC and lack of apparent intoxication suggests
tolerance
Blood Alcohol Concentration (BAC)
Questionnaire Based Assessment for Alcohol Abuse
1. Alcohol Use Disorder Identification Tool (AUDIT)
Is a simple ten question test develop by WHO to determine if a person’s alcohol
consumption may be harmful
Question 1 – 3 deal with alcohol consumption, 4 – 6 relate to alcohol dependence
and 7 – 10 consider alcohol-related problems
A score of 8 or more in men (7 in women) indicates a strong likelihood of
hazardous or harmful alcohol consumption
A score of 20 or more is suggestive of alcohol dependence (some authors quotes
scores of more than 13 in women and 15 in men indicating likely dependence)
Questionnaire Based Assessment for Alcohol Abuse
Questionnaire Based Assessment for Alcohol Abuse

2. CAGE questionnaire
C – “have you ever felt you should cut down on your drinking”?
A – “have people annoyed you by criticizing your drinking”?
G – “have you ever felt bad or guilty about your drinking”?
E – eye opener: “have you ever had a drink first thing in the morning to steady your
nerves or to get rid of a hangover’?

Two “yes” answers to CAGE test indicates problems with alcohol

Alcohol intoxication (DSM-5 criteria)
A. Recent ingestion of alcohol
B. Clinically significant problematic behavioural and psychological changes (e.g., inappropriate
sexual or aggressive behavior, mood lability, impaired judgement) that developed during, or
shortly after, alcohol ingestion.
C. One (or more) of the following signs or symptoms developing during, or shortly after
alcohol use:
i. Slurred speech
ii. Incoordination
iii. Unsteady gait
iv. Nystagmus
v. Impairment in attention or memory
vi. Stupor or coma
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication with another substance.
Alcohol withdrawal syndrome (DSM-5 criteria)
A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged
B. Two (or more) of the following, developing within several hours to a few days after the
cessation of (or reduction in) alcohol use described in Criterion A:
i. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm)
ii. Increased hand tremor
iii. Insomnia
iv. Nausea or vomiting
v. Transient visual, tactile, or auditory hallucinations, or illusions
vi. Psychomotor agitation
vii. Anxiety
viii. Generalized tonic-clonic seizures
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning
Alcohol withdrawal syndrome (DSM-5 criteria)

D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance

Specify if:
With perceptual disturbances: This specifier applies in the rare instance when
hallucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual,
or tactile illusions occur in the absence of a delirium
 DELIRIUM TREMENS?
A medical emergency; mortality of 10-20% if left untreated.
Alcohol withdrawal delirium: This diagnosis should be made instead of alcohol
withdrawal when the symptoms in Criteria A & C predominate in the clinical picture
& when they are sufficiently severe to warrant clinical attention.
Criteria A: A disturbance in attention (i.e., reduced ability to direct, focus,
sustain & shift attention) & awareness (reduced orientation to the environment).
Criteria C: An additional disturbance in cognition (e.g., memory deficit,
disorientation, language, visuospatial ability, or perception).
72-96 hours after the cessation of heavy drinking.
Positive history of alcohol misuse which extends over several years.
Features:
Clouding of consciousness, disorientation in time & place, and impairment of recent
memory.
Misinterpretations of sensory stimuli & vivid hallucinations (visual & tactile).
Agitation/ restlessness/ tremulousness.
Insomnia.
Autonomic hyperactivity (hyperhidrosis, fever, tachycardia, raised BP, mydriasis).
Metabolic disturbance (dehydration, electrolyte imbalance).
Blood test (leucocytosis, impaired liver function).
Characteristically worse at night & often ends with a
deep, prolonged sleep from which the patient awakens
with no symptoms & little/ no memory of the delirium.
Management:
Prompt transfer to a general medical setting.
IV benzodiazepines, i.e. diazepam.
IV Pabrinex.
IV fluids (correction of electrolyte imbalance & dehydration due to
diaphoresis & fever).
Antipsychotics such as haloperidol are useful to manage
hallucinations & agitation (be aware of the risk of hypotension,
QTc prolongation, and reduced seizure threshold. Have
parenteral procyclidine available in case of dystonic reactions).
Full delirium investigations (rule out organic causes).
Physically restraining patients is risky as they may fight against
the restraints to a dangerous level of exhaustion. When they are
uncontrollable, a seclusion room can be used.
 MANAGEMENT

Relapse
Alcohol
prevention
detoxification
 DETOXIFICATION
Pharmacologically assisted withdrawal is likely to be necessary when:
Regular consumption of >15 units/ day.
AUDIT score >20.
A history of significant withdrawal symptoms.
To determine the amount of pharmacological support needed to manage a patient’s
withdrawal symptoms:
CIWA-Ar score >10, or Should prompt assisted
SAWS score >12. withdrawal!‌
·Benzodiazepines are the treatment of choice for alcohol withdrawal.
Chlordiazepoxide is the choice in UK.
Cross-tolerance with alcohol & have anticonvulsant properties.
A relatively low dependence-forming potential.
Taylor, D. M., Barnes, T. R. E., & Young, A. H. (2018). The Maudsley prescribing guidelines in psychiatry (13th ed.). John Wiley & Sons.
Taylor, D. M., Barnes, T. R. E., & Young, A. H. (2018). The Maudsley prescribing guidelines in psychiatry (13th ed.). John Wiley & Sons.
 RELAPSE PREVENTION
Benzodiazepines are NOT for relapse prevention.
Please ensure that the patients have gone through the detoxification process or do not
have any significant withdrawal symptoms.
Acamprosate – acts as a functional glutamatergic NMDA antagonist & increases
GABAergic function.
Naltrexone – a non-selective opioid receptor antagonist which prevents dopaminergic
activity after the consumption of alcohol, thus reducing its rewarding effects &
significantly reduces relapse.
Disulfiram – inhibits aldehyde dehydrogenase, thus preventing the complete
metabolism of alcohol in the liver; causes the accumulation of acetaldehyde inside the
body which causes the alcohol-disulfiram reaction (e.g., facial flushing, sweating,
nausea, dyspnoea, tachycardia, etc.). The incompatibility of disulfiram with alcohol
causes a strong aversion to alcohol.
Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan and Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed.). Wolters Kluwer Health.
 People who join this fellowship gather to address their drinking
issue.
Expansive network across the USA, Canada, and other countries
Alcoholic including Indonesia and Singapore.
Goal: To assist alcoholics in becoming sober.
Anonymous? Twelve Steps:
We admitted we were powerless over alcohol — that our lives
had become unmanageable.
Came to believe that a Power greater than ourselves could
restore us to sanity.
Made a decision to turn our will and our lives over to the care of
God as we understood Him.
Made a searching and fearless moral inventory of ourselves.
Admitted to God, to ourselves, and to another human being the
exact nature of our wrongs.
Were entirely ready to have God remove all these defects of
character.
Humbly asked Him to remove our shortcomings.
Made a list of all persons we had harmed and became willing to
make amends to them all.
Made direct amends to such people wherever possible, except
when to do so would injure them or others.
Continued to take personal inventory and when we were wrong
promptly admitted it.
Sought through prayer and meditation to improve our conscious
contact with God as we understood Him, praying only for
knowledge of His will for us and the power to carry that out.
Having had a spiritual awakening as the result of these Steps, we
tried to carry this message to alcoholics, and to practice these
principles in all our affairs.
 Stages of change &
motivational interviewing (MI)?
Transtheoretical Model of Behaviour Change
(Prochaska & DiClemente)
Readiness for change
Mediates behavioural change.
Dynamic process influenced by pros and cons of change,
creating ambivalence.
Ambivalence
A conflicted state.
Common in situations with immediate rewards vs. long-term
consequences (e.g., substance abuse, weight management).
Hall, K., Gibbie, T., & Lubman, D. (2012). Motivational interviewing techniques facilitating behaviour change in the general practice setting. Australian Family Physician, 41(9), 660–667.
https://www.racgp.org.au/getattachment/1564cfd0-c1d4-4ab6-9e29-4205ffefdc85/Motivational-interviewing-techniques.aspx
 Motivational interviewing (MI)
A counselling technique that enhances motivation by resolving ambivalence.
Developed from the Stages of Change model and addiction medicine.
Three critical components of motivation (Miller & Rollnick)
Willingness: Importance of change for the individual.
Ability: Confidence to make the change.
Readiness: Whether change is an immediate priority.
The practical application of MI occurs in two phases:
Building motivation to change.
Strengthening commitment to change.
Four guiding principles of MI: RULE
Resisting the righting reflex.
Understanding the patient’s motivation.
Listening with empathy.
Empowering your patient.
Other Substance
Disorders
Opioids MOA
Full/strong agonist
Opioids act by binding to the opioid
- Morphine (Miss Emma)
receptors in the CNS; release
- Methadone (Fizzies)
- Pethidine endogenous opioid peptide (activation of
- Fentanyl (Chinaa White, Dance fever) opioid receptor)
- Oxycodone (Oxy, Percs)
- Heroin (Horse, Smack) Inhibit neuronal activity by
1. Postsynaptic hyperpolarization by
Partial/moderate agonist increasing K+ efflux (open K+ channel)
- Codeine, Buprenorphine and decrease response to excitatory NT
2. Reduces presynaptic Ca2+ influx
Mixed Agonist-Antagonist (inhibit opening of Ca2+ channel);
- Nalbuphine
decrease release of excitatory NT;
glutamate
Opioid Antagonist
- Naloxone, Naltrexone
Opioids
Routes of admission

Oral (pills, syrups): Most prescribed opioids are taken orally.

Intravenous (IV): Injection into veins is common for rapid effects
(e.g., heroin).
Intranasal (snorting): Often used for heroin, oxycodone.
Inhalation (smoking): Fentanyl and heroin can be smoked.
Transdermal: Fentanyl patches
 Opioids Intoxication Features
A. Recent use of an opioid.

B. Clinically significant problematic behavioral or psychological changes (e.g., initial euphoria

followed by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment) that
developed during, or shortly after, opioid use.

C. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and one (or
more) of the following signs or symptoms developing during, or shortly after, opioid use:
1. Drowsiness or coma.
2. Slurred speech.
3. Impairment in attention or memory.

D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance.
 Opioids Withdrawal features
A. Presence of either of the following:
C. The signs or symptoms in Criterion
1. Cessation of (or reduction in) opioid use that has
B cause clinically significant
been heavy and prolonged (i.e., several weeks or
distress or impairment in social,
longer).
occupational, or other important areas
2. Administration of an opioid antagonist after a
of functioning.
period of opioid use.
D. The signs or symptoms are not
attributable to another medical
B. Three (or more) of the following developing within
condition and are not better explained
minutes to several days after Criterion A:
by another mental disorder, including
1. Dysphoric mood. 5. Pupillary
intoxication or withdrawal from
dilation, piloerection, or sweating.
another substance.
2. Nausea or vomiting. 6. Diarrhea
3. Muscle aches. 7. Yawning
4. Lacrimation or rhinorrhea. 8. Fever
9. Insomnia
Opioids
Investigation

Urine Drug Screen (UDS):

Heroin: Detectable for 1-4 days in urine.
Morphine: Detectable for 2-3 days in urine.
Fentanyl: Detectable for up to 3 days.

Blood Tests: Detect opioids for shorter periods (up to 24 hours).

Hair Drug Testing: Can detect opioid use for up to 90 days.
Opioids
Management

Withdrawal management
Pharmacological intervention
Methadone (full agonist)
Acute overdose
A long acting opioid, used in opioid
Naloxone (Full antagonist)
replacement therapy (mimics heroin)
Treatment for opioid overdose by
in detoxification phase
displacing full agonist from
receptor
Naltrexone (reversible
antagonist)
Prevent relapse after detoxification
Given after 7-10 days being opioid
free
Opioids
Management

Psychological management Harm reduction

Cognitive Behavioral Education: Informing individuals about
Therapy (CBT): Helps safe drug use practices, overdose risks,
patients recognize and and available treatments.
change addictive
behaviors and coping
mechanism
Support groups:
Narcotics Anonymous
(NA), group therapy,
family therapy.
 Hallucinogen Mechanism of Action (MOA)
Phencyclidine (PCP):
PCP:
Street names: "Angel Dust," "Rocket Fuel,"
PCP works primarily as an NMDA receptor
Other Hallucinogens:
antagonist, disrupting the normal activity of
LSD (Lysergic Acid Diethylamide): Street
glutamate, which plays a crucial role in mood,
names: "Acid," "Blotter."
perception, and pain regulation. This leads to
Psilocybin: Found in magic mushrooms,
dissociative and hallucinogenic effects.
street names: "Shrooms," "Mushies."
Other Hallucinogens:
Mescaline: Derived from peyote cactus,
LSD, Psilocybin, Mescaline, and DMT act
street names: "Peyote," "Buttons."
mainly on serotonin (5-HT2A) receptors,
MDMA (Ecstasy): A stimulant with
altering perception, mood, and thought
hallucinogenic properties, street names:
processes. These drugs distort sensory
"Molly," "E."
perception and produce vivid hallucinations.
DMT (Dimethyltryptamine): Street names:
"Dimitri," "Businessman’s Trip."
Hallucinogen
Routes of Admission

Oral: Pills, tablets, or liquid forms for LSD, psilocybin, and MDMA.
Intranasal (Snorting): Common for PCP and DMT.
Smoking: PCP and DMT are commonly smoked.
Intravenous (IV): Less common but used for rapid effects in PCP
and DMT.
 Hallucinogen
Intoxication Features (PCP)
C. Within 1 hour, two (or more) of the following
A. Recent use of phencyclidine
signs or symptoms:
(or a pharmacologically similar
Note: When the drug is smoked, “snorted,” or
substance).
used intravenously, the onset may be
B. Clinically significant
particularly rapid.
problematic behavioral changes
1. Vertical or horizontal nystagmus.
(e.g., belligerence, assaultive-ness,
2. Hypertension or tachycardia.
impulsiveness, unpredictability,
3. Numbness or diminished responsiveness to
psychomotor agitation, impaired
pain.
judgment) that developed during, or
4. Ataxia.
shortly after, phencyclidine use.
5. Dysarthria.
6. Muscle rigidity.
7. Seizures or coma.
8. Hyperacusis.
 Hallucinogen
Intoxication Features (Other than PCP)
A. Recent use of a hallucinogen (other than D. Two (or more) of the following signs
phencyclidine). developing during, or shortly after, hallucinogen
B. Clinically significant problematic use:
behavioral or psychological changes (e.g., 1. Pupillary dilation.
marked anxiety or depression, ideas of 2. Tachycardia.
reference, fear of “losing one’s mind,” paranoid 3. Sweating.
ideation, impaired judgment) that developed 4. Palpitations.
during, or shortly after, hallucinogen use. 5. Blurring of vision.
C. Perceptual changes occurring in a state of 6. Tremors.
full wakefulness and alertness (e.g., subjective 7. Incoordination.
intensification of perceptions, depersonalization, E. The signs or symptoms are not attributable to
derealization, illusions, hallucinations, another medical condition and are not better
synesthesias) that developed during, or shortly explained by another mental disorder, including
intoxication with another substance.
after, hallucinogen use.
Hallucinogen
Withdrawal Features

Hallucinogens, including LSD and psilocybin, do not typically

produce physical dependence or withdrawal symptoms. However,
users may experience hallucinogen persisting perception disorder
(HPPD), where flashbacks or persistent perceptual disturbances
occur long after the drug has worn off.
PCP withdrawal: Can lead to symptoms such as confusion,
depression, and cravings, although physical withdrawal is less
common.
Hallucinogen
Hallucinogen Persisting Perception Disorder

A. Following cessation of use of a B. The symptoms in Criterion A cause

hallucinogen, the reexperiencing of clinically significant distress or
one or more of the perceptual impairment in social, occupational, or
symptoms that were experienced other important areas of functioning.
while intoxicated with the hallucinogen
(e.g., geometric hallucinations, false C. The symptoms are not attributable to
perceptions of movement in the another medical condition (e.g., anatomical
peripheral visual fields, flashes of color, lesions and infections of the brain, visual
intensified colors, trails of images of epilepsies) and are not better explained by
moving objects, positive afterimages, another mental disorder (e.g., delirium,
halos around objects, macropsia and major neurocognitive disorder,
micropsia). schizophrenia) or hypnopompic
hallucinations.
Hallucinogen
Investigation
Urine Drug Screen (UDS):
PCP: Detectable in urine for up to 7-14 days after use.
LSD: Detectable in urine for up to 1-3 days, though testing is rare due to
its rapid clearance and low concentrations.
MDMA: Detectable for 1-3 days in urine.

Blood Tests: Shorter detection window (24 hours for most hallucinogens).

Psychiatric Evaluation: In cases of prolonged psychosis or HPPD,

psychiatric assessment is crucial to differentiate drug-induced conditions
from other psychiatric disorders.
 Hallucinogen
Management

Pharmacological Intervention:
Acute PCP intoxication:
1. Benzodiazepines (e.g., lorazepam, diazepam): Used to manage agitation, seizures,
and muscle spasms.
2. Antipsychotics (e.g., haloperidol): May be used for severe agitation or psychosis,
though their use is controversial as they can worsen the dissociative effects of PCP.

For other hallucinogens:

1. Benzodiazepines: To calm patients experiencing a "bad trip" (anxiety, panic, and
agitation).
2. No specific antidotes exist for LSD, psilocybin, or MDMA intoxication. Treatment focuses
on supportive care and symptomatic management (hydration, rest).
 Hallucinogen
Management
Psychological Management:
Cognitive Behavioral Therapy (CBT): Harm Reduction:
Addresses maladaptive thinking patterns that Education: Raising awareness about the
contribute to continued drug use and helps unpredictable effects of hallucinogens,
individuals cope with cravings or flashbacks. particularly in the context of mental health
Motivational Interviewing (MI): Supports conditions or when using potent substances
behavior change by exploring the individual’s like PCP.
motivations for using hallucinogens and Trip sitting: A harm reduction strategy
helping them find reasons to quit. where a sober individual stays with the user
Psychoeducation: Informs users about the to guide them through the experience and
risks of hallucinogen use and coping prevent injury or panic.
mechanisms for managing HPPD or anxiety
post-use.
 Stimulant
Amphetamines: Mechanism of Action (MOA)
1. Methamphetamine: Street names: "Ice," "Crystal,"
Amphetamine: indirect monoamine
"Glass."
agonist that produce the release of
2. Amphetamine: Street names: "Speed," "Uppers."
norepinephrine, dopamine, and serotonin
in both the CNS and periphery. "
Cocaine: Street names: "Coke," "Blow," "Snow."
Cocaine: binds and blocks monoamine
MDMA (3,4-methylenedioxy- and reuptake transporters with equal
methamphetamine): Street names: "Ecstasy," affinity
"Molly." MDMA: acts as a releasing agent and
reuptake inhibitor
Prescription Stimulants:
1. Methylphenidate (Ritalin), Adderall: Used
medically for ADHD but misused recreationally:
Street names: "Ritz," "Skippy."
Stimulant
Routes of Admission

Oral: Pills (e.g., ecstasy, prescription stimulants like Adderall or

Ritalin).
Snorting (Intranasal): Common with cocaine and
methamphetamine.
Smoking: Methamphetamine ("Ice"), crack cocaine.
Intravenous (IV): Methamphetamine and cocaine can be
injected for a more intense high.
 Stimulant
Intoxication Features
A. Recent use of an amphetamine-type C. Two (or more) of the following signs or
substance, cocaine, or other stimulant. symptoms, developing during, or shortly after,
stimulant use:
B. Clinically significant problematic 1. Tachycardia or bradycardia.
behavioral or psychological changes 2. Pupillary dilation.
(e.g., euphoria or affective blunting; 3. Elevated or lowered blood pressure.
changes in sociability; hypervigilance; 4. Perspiration or chills.
interpersonal sensitivity; anxiety, tension, 5. Nausea or vomiting.
or anger; stereotyped behaviors; 6. Evidence of weight loss.
impaired judgment) that developed 7. Psychomotor agitation or retardation.
during, or shortly after, use of a 8. Muscular weakness, respiratory depression,
stimulant. chest pain, or cardiac arrhythmias.
9. Confusion, seizures, dyskinesias, dystonias, or
coma.
 Stimulant Withdrawal Features
A. Cessation of (or reduction in)
C. The signs or symptoms in
prolonged amphetamine-type substance,
Criterion B cause clinically
cocaine, or other stimulant use.
significant distress or
B. Dysphoric mood and two (or more) of
impairment in social,
the following physiological changes,
occupational, or other important
developing within a few hours to several
areas of functioning.
days after Criterion A:
1. Fatigue.
D. The signs or symptoms are not
2. Vivid, unpleasant dreams.
attributable to another medical
3. Insomnia or hypersomnia.
condition and are notbetter
4. Increased appetite.
explained by another mental
5. Psychomotor retardation or agitation.
disorder, including intoxication or
withdrawal from another
substance.
Stimulant
Investigation

Urine Drug Screen (UDS):

Cocaine: Detectable in urine for up to 1-3 days with single
dose, and 7-12 days in usage with repeated high dose.
Methamphetamine: Detectable in urine for up to 1-3 days.
MDMA: Detectable in urine for 1-3 days.

Hair Drug Testing: Can detect amphetamine type stimulant use

for up to 90 days.
 Stimulant
Management

Pharmacological Intervention:
Acute intoxication:
1. Benzodiazepines: To reduce agitation, anxiety, and prevent seizures.
2. Antipsychotics (e.g., haloperidol): To manage stimulant-induced
psychosis.

Withdrawal management:
No specific medications approved for stimulant withdrawal
 Stimulant
Management
Psychological Management:
Cognitive Behavioral Therapy (CBT):
Effective in addressing distorted Harm Reduction
thinking patterns and preventing Education: Informing users of
relapse. the dangers of stimulant use,
Contingency Management: Providing including overdose risks and
rewards for abstaining from drug use. unsafe injection practices
Group therapy: Involving peer support
and sharing recovery experiences.
Motivational Interviewing (MI): Helps
individuals develop the motivation to
quit stimulant use.
Sedatives, Hypnotics and Anxiolytics
Mechanism of action
Benzodiazepines and non-benzodiazepine hypnotics:
Act on the GABA-A receptors by enhancing the effect of the
inhibitory neurotransmitter gamma-aminobutyric acid (GABA),
leading to sedative, anxiolytic, muscle relaxant, and
anticonvulsant effects.
Non-benzodiazepine hypnotics (e.g., zolpidem) act selectively
on the GABA-A receptors, causing fewer side effects
compared to benzodiazepines.

Barbiturates:
Potentiate the action of GABA at the GABA-A receptors but at
a different site compared to benzodiazepines. They have a
stronger sedative effect and a much narrower therapeutic
window, making overdose more dangerous.

Route of Administration
Oral
Intravenous
Intramuscular
 Intoxication

A. Recent use of a sedative, hypnotic, or anxiolytic.

B. Clinically significant maladaptive behavioral or psychological changes (e.g., inappropriate
sexual or aggressive behavior, mood lability, impaired judgment) that developed during, or
shortly after, sedative, hypnotic, or anxiolytic use.
C. One (or more) of the following signs or symptoms developing during, or shortly after,
sedative, hypnotic, or anxiolytic use:
1. Slurred speech.
2. Incoordination.
3. Unsteady gait.
4. Nystagmus.
5. Impairment in cognition (e.g., attention, memory).
6. Stupor or coma.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disor-der, including intoxication with another substance.
 Withdrawal
A. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been prolonged.
B. Two (or more) of the following, developing within several hours to a few days after the
cessation of (or reduction in) sedative, hypnotic, or anxiolytic use described in Criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
2. Hand tremor.
3. Insomnia.
4. Nausea or vomiting
5. Transient visual, tactile, or auditory hallucinations or illusions.
6. Psychomotor agitation.
7. Anxiety.
8. Grand mal seizures.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication or withdrawal from another
substance.
 Investigation
1. Urine Toxicology Screening
Most common test for detecting the presence of sedatives, hypnotics, and anxiolytics.
Benzodiazepines:
Detectable in urine for 3–30 days, depending on the half-life of the drug:
Short-acting benzodiazepines (e.g., alprazolam, lorazepam): 3-5 days.
Long-acting benzodiazepines (e.g., diazepam, clonazepam): up to 30 days due to accumulation of
metabolites.
Barbiturates:
Detectable for 4–7 days for short-acting barbiturates (e.g., secobarbital) and up to 3–4 weeks for long-
acting barbiturates (e.g., phenobarbital).
Non-benzodiazepine hypnotics (Z-drugs):
Short detection windows, detectable in urine for 1–2 days (e.g., zolpidem, eszopiclone).

2. Blood Testing
Used for recent use or in cases of overdose where rapid detection is necessary.
Benzodiazepines:
Detectable in blood for hours to a few days, depending on the drug's half-life:
Short-acting (e.g., alprazolam): up to 12–24 hours.
Long-acting (e.g., diazepam): up to 48–72 hours or more.
Caffeine
A bitter substance that occurs naturally in more than 60 plants such
as coffee beans, tea leaves, kola nuts, cacao pods, and many more
Naturally occurring central nervous system which belongs to
methylxanthine
Widely recognized as most utilized psychoactive stimulant
worldwide.

Mechanism of action
Adenosine receptors antagonist which specifically bind to A1 and
A2A receptors. (increases alertness and reduces drowsiness)
Dopaminergic modulation. (enhances mood and reward response)
Sympathetic activation (increase hr, bp, and energy availability)
Calcium release (improves muscle contractility and physical
performance)
Route of administration
Caffeine is also used in various cosmetic
products and can be administered topically,
orally, by inhalation, or by injection.
It has nearly 100% oral bioavailability and is the
primary administration router.

Pharmacokinetics
half-life of caffeine in the average adult is approximately
5 hours, multiple factors can influence the metabolism
and duration. In smokers, the half-life is reduced by up to
50% compared to nonsmokers. Conversely, pregnant
patients, especially in the final trimester, may experience
a prolonged half-life of up to 15 hours.
 Intoxication features
Recent consumption of caffeine (> 250mg)
5 (or more signs) or symptoms developing during, or shortly after, use:
1. Restlessness
2. Nervousness
3. Excitement
4. Insomnia
5. Flushed face
6. Diuresis
7. GI disturbance
8. Muscle twitching
9. Rumbling flow of thought and speech
10. Tach or cardiac arrhythmia
11. Periods of inexhaustibility
12. Psychomotor agitation
S&S cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning
S&S is not attributed to another medical condition or not better explained by other mental
disorders, including intoxication with other substances
 Withdrawal features
Prolonged daily use of caffeine
Abrupt cessation of or reduction in caffeine use, followed within 24
hours by 3 (or more) of the following signs or symptoms:
1. Headache
2. Marked fatigue or drowsiness
3. Dysphoric mood, depressed mood, or irritability
4. Difficulty concentrating
5. Flu-like symptoms (nausea, vomiting, or muscle pain/stiffness)

S&S cause clinically insignificant distress or impairment in social,

occupational, or other important areas of functioning.
S&S are not associated with the physiological effects of another
medical condition (e.g., migraine, viral illness)
 Investigation

FBC to evaluate for infection. Although caffeine toxicity can be present, infectious processes should
be excluded.
BUSE + Cretinine. Hypokalemia is a classic feature of caffeine overdose. An increased anion gap
(resulting from lactic acidosis) and hyperglycemia are also common findings in severe toxicity.
Total creatine kinase (CK) concentrations to check for rhabdomyolysis, which is occasionally
associated with severe caffeine toxicity. A CK concentration greater than 5 times the upper limit of
normal indicates clinically significant rhabdomyolysis.
Urine dipstick to look for rhabdomyolysis, myoglobinuria, or both. Glucosuria and ketonuria are also
common findings.
A rapid urine drug screen may help in identifying co-ingested substances. Illicit drugs, such as
ecstasy or methamphetamine, often contain caffeine as a substitute or co-ingredient.
 Management
Pharmacological Intervention

Mild to Moderate Intoxication Severe Intoxication

manage severe reduce further absorption of
Activated charcoal
agitation, anxiety, or caffeine from GT tract
Benzodiazepines tremors resulting
from caffeine correct dehydartion and
overuse (lorazepam) Intravenous fluids enhance renal excreation of
caffeine
control caffeine-
induced tachycardia,
Beta-blockers
hypertension, and
palpitations indicated in life-threatening
Magnesium sulfate
arrythmias

Alleviate nausea and

Antiemetics
vomiting
 Psychosocial Management
Cognitive-behavioral therapy (CBT ) useful for
addressing the psychological dependence on caffeine.
Behavioral Therapy Motivational interviewing (MI) used to enhance the
patient’s motivation for reducing or quitting caffeine,
especially if they’re ambivalent about change.

Help the individual develop better ways to cope with stress,

Stress management
including mindfulness, meditation, and other stress-relief
techniques, reducing the need for caffeine as a coping
mechanism.

Education about sleep hygiene is essential, as poor sleep is

Sleep hygiene
often a reason for excessive caffeine consumption.
Encourage regular sleep schedules, minimizing screen time
before bed, and creating a relaxing bedtime routine.
 Harm Reduction

Gradual Tapering:
1. Reduce caffeine consumption gradually
2. Substitutes for caffeine

Education
1. Inform about safe caffeine consumption
2. Encourage monitoring caffeine intake

Support Network
Tobacco
Tobacco is a plant with stimulant effects. Nicotine is one of the
many naturally occurring chemicals found in tobacco,
Types
Cigarettes
Cigars
Smokeless tobacco (chewing tobacco, snuff)
E-cigarettes/vapes (liquid nicotine)

Mechanism of Action
Tobacco contains nicotine, an alkaloid that primarily acts on the nicotinic acetylcholine
receptors (nAChRs) in the brain. Nicotine stimulates these receptors, causing the release of
neurotransmitters such as dopamine, leading to feelings of pleasure, reward, and
addiction. Nicotine also affects other neurotransmitters, including norepinephrine and
serotonin, which contribute to mood regulation and alertness.
 Investigation
Route of Administration 1. Urine Testing
Inhalation Most common method to detect nicotine and its metabolite cotinine.
Nicotine:
(absorbed through Detectable in urine for 2-4 days after tobacco use.
the lungs into the Cotinine (the primary metabolite of nicotine):
Detectable in urine for up to 3-4 weeks after cessation due to its
bloodstream) longer half-life.
Buccal/mucosal Urine tests are used because cotinine concentrations are typically higher
in urine than in other bodily fluids, making detection easier.
absorption:
(absorbed through 2. Blood Testing
Used to detect nicotine and cotinine levels, especially in clinical or
the oral mucosa) forensic settings.
Transdermal Nicotine:
Detectable in blood for 1-3 days after tobacco use.
patches Cotinine:
Detectable in blood for up to 10 days.
Blood testing provides precise measurements of current nicotine
exposure, which can be used for clinical assessment or smoking
cessation programs.
 Intoxication Features
A. A problematic pattern of tobacco use leading to clinically significant impairment or distress, as manifested by at least two
of the following, occurring within a 12-month period:
1. Tobacco is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control tobacco use.
3. A great deal of time is spent in activities necessary to obtain or use tobacco.
4. Craving, or a strong desire or urge to use tobacco.
5. Recurrent tobacco use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., interference with
work).
6. Continued tobacco use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by
the effects of tobacco (e.g., arguments with others about tobacco use).
7. Important social, occupational, or recreational activities are given up or reduced because of tobacco use.
8. Recurrent tobacco use in situations in which it is physically hazardous (e.g., smoking in bed).
9. Tobacco use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is
likely to have been caused or exacerbated by tobacco.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of tobacco to achieve the desired effect.
b. A markedly diminished effect with continued use of the same amount of tobacco.

11. Withdrawal, as manifested by either of the following:

a. The characteristic withdrawal syndrome for tobacco (refer to Criteria A and B of the criteria set for tobacco withdrawal).
b. Tobacco (or a closely related substance, such as nico-tine) is taken to relieve or avoid withdrawal symptoms.
Withdrawal Features
A. Daily use of tobacco for at least several weeks.
B. Abrupt cessation of tobacco use, or reduction in the amount of tobacco used,
followed within 24 hours by four (or more) of the following signs or symptoms:
1. Irritability, frustration, or anger.
2. Anxiety.
3. Difficulty concentrating.
4. Increased appetite.
5. Restlessness.
6. Depressed mood.
7. Insomnia.
C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disor-der, including intoxication or withdrawal from
another substance.
Management
Cannabis
Cannabis produced from dried leaves, flowers, stems and seeds of
Cannabis Sativa
Most commonly used illegal drugs
May be smoked in cigarettes, alone, or mixed and Resin form
(Hash) can be eaten directly or mixed into foodstuffs (e.g. Cakes)
Contain at least 60 psychoactive cannaboids, in which the most
important is 9-δ- Tetrahydrocannabinol (THC)

Type Street Drug name /Slang

Cannabis Blow, Dope, Grass, Hash, Marijuana, Skunk (Potent form of Cannabis)

Cannabis cigarette Spliff

 Route of administration
Smoking (cigarette)
Oral ingestion (directly or incorporated into dish)

Mechanism of action
Activate cannabinoid receptor causing inhibition of adenylate
cyclase, subsequent decrease in intracellular cAMP concentration,
and inhibition of neurotransmission. 2 subtypes of cannabinoid
receptors :
Receptor highly located in Hippocampus, Basal ganglia,
Cerebellum and spinal cord
Responsible for memory, movement, appetite, metabolism and
immunity/ inflammatory functions (CB2)
 DSM 5 Diagnostic Criteria of Cannabis Intoxication

A. Recent use of Cannabis

B. Clinically significant problematic behavioral or physiological changes (e.g. Euphoria, impaired
judgement) developed during or shortly after usage of cannabis
C. ≥2 of following signs or symptoms developing within 2 hours of cannabis usage:
Conjunctival injection
Increased appetite
Dry mouth
Tachycardia
D. Signs or symptoms are not attributable to other medical condition and not better explained by
other mental disorder, including intoxication of other substance.
 DSM 5 Diagnostic Criteria of Cannabis Withdrawal
A. Cessation of cannabis use that has been heavy and prolonged (e.g. usually daily or almost
daily use over a period at least a few months)
B. ≥3 of the following signs and symptoms develop within approximately 1 week after criterion
A:
Irritability, anger or aggression
Nervousness or anxiety
Sleep difficulty
Decreased appetite or weight loss
Restlessness
Depressed mood
≥1 of following physical symptoms causing discomfort :
Abdominal pain
Tremors
Sweating
Fever
Chills
Headache
 DSM 5 Diagnostic Criteria of Cannabis Withdrawal

C. Signs or symptoms in criterion B cause clinically significant distress or impairment in

social, occupational, or other important areas of functioning
D. Signs or symptoms are not attributable to other medical condition and are not explained by
other mental disorder, including intoxication or withdrawal from other substance
 Investigation

Urine toxicology
cannabinoid can be detected in urine for 21 days after usage
Salivary test
The presence of delta-9-THC in oral fluid is a better indication of recent use than the
presence of 11-nor-delta-9-THC-9-COOH detected in urine.
Full blood count
To measure quantitative levels of cannabinoid
Monitoring of tetrahydrocannabinol to creatinine ratios can distinguish recent use and
residual excretion
 Management
By achieving Abstinence and Support
Abstinence - Monitoring by urine drug screens (outpatient) or Hospitalization (If
necessary)

Biological
Antianxiety drug- short term relief of withdrawal symptoms
Psychosocial
Psychoeducation for patient and family members
Educate regarding the effects of abusing substances on physical and mental health
Encourage support from family members towards abstinence
Cognitive behaviour therapy (CBT)
Helps patient to think positively towards the process of withdrawal and abstinence.
Gradually change the behaviour of the patient by changing their ways of thinking
Social skill training
Group psychotherapies
 Inhalants
Inhalant drugs also known as volatile substances or solvents and also a volatile
hydrocarbons
Compounds that are commonly found in many household products that can be divided into
4 commercial classes:
Glues & adhesives
Propellant (e.g. Aerosol paint sprays, hair sprays)
Thinners
Fuels (e.g. Gasoline, propane)
Associated with conduct disorder, mood disorders, suicide cases and physical and sexual
abuse
Commonly found in adults and lower socioeconomic groups
Inhalants (Street name & Terms)

Usage term:
Bagging/ Huffing/ Glading - using inhalants
Bang - to inject inhalant
Bullet bolt/ Highball/ Air blast - term for inhalants

Specific inhalant name:

Amphetamine -Aimies, Bolt
Isobutyl nitrite -Bolt, Bullet, Poppers, Quicksilver, Whiteout
Amyl nitrite -Aimies, Poppers
Snotballs - Rubber cement rolled into balls, burned and inhaled fumes
Route of administration
Inhalation :
Sniffing
Lead to transpulmonary
Huffing
absorption with very rapid
Bagging
drug access to the brain
Inhaling
Spraying

Mechanism of action
Its effects are not well understood however inhalants have similar effects and additive effects
as other CNS depressants (EtOH, Barbiturates and BDZ)
Research suggested it operate by enhancing GABA system
Some suggested it work through membrane fluidization ( similar to pharmacodynamic effect
of ethanol)
 DSM-5 criteria of Inhalant Intoxication
A. Recent exposure to high dose substances ( incl Volatile hydrocarbons such as toluene or
gasoline) in short term either with intention or without intention.
B. Clinically significant problematic behavioural or psychological changes that developed during,
or shortly after the exposure to inhalants ( e.g. Impaired judgement, belligerence, assaultiveness)
C. ≥2 of following signs or symptoms developing during, or shortly after to inhalant use or
exposure:
Dizziness
Nystagmus
Incoordination
Slurred speech
Unsteady gait
Lethargy
Depressed reflexes
Psychomotor retardation
Tremor
Generalized muscle weakness
 DSM-5 criteria of Inhalant Intoxication (cont.)
C. ≥2 of following signs or symptoms developing during, or shortly after to inhalant use or
exposure:
Blurred vision or diplopia
Stupor or coma
Euphoria
D. Signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance
 Inhalant Withdrawal
The effects of inhalant withdrawals can cause series of uncomfortable symptoms especially
those who have been continuosly abusing inhalant, suddenly stopping or reducing :

Agitation and irritability

Headaches
Nausea
Excessive sweating
Tremors and convulsions
Abdominal cramping
Intense cravings
 Investigation
Pulse oximetry
To assess the degree of oxygenation and general state of pulmonary function
Arterial blood gases
To assess severity of inhalant intoxication
Full blood count
Routine screening test. Chronic patient may exhibit bone marrow suppression,
thrombocytopenia or aplastic anaemia
Serum/ Urine toxicology
Toxicology screens may be helpful if the specific chemical involved is unknown.
Toluene can be detected as urinary hippuric acid (UHA) but required correlation to blood
toluene levels
Creatine phosphokinase
Useful in patients with muscle tenderness or myoglobinuria to evaluate the presence of
rhabdomyolysis.
Urine pregnancy test
should be done in all solvent-abusing females because of the risk of embryopathy caused
by these agents.
 Management (Psychosocial)

Cognitive behavior therapy (CBT)

CBT includes teaching how to handle stressful situations, coping with cravings and
resisting offers to use inhalants.
Motivational interventions:
This counseling style helps teens gain the motivation to commit to change.
Family counseling:
This therapy focuses on improving communication, relationships, actions and behaviors
between family members.
Activity and engagement programs:
These programs provide new skills and social experiences and offer an alternative to
inhalant use. Programs include activities such as movie nights, dances, hiking and more.
These types of programs play an important role in maintaining a substance-free life by
helping teens engage in new social relationships with others who are non-users.
New Psychoactive Substances
What is New Psychoactive Substances???
defined as “substances of abuse, either in a pure form or a preparation that are not controlled by
the 1961 Single Convention on Narcotic Drugs or the 1971 Convention on Psychotropic
Substances, but which may pose a public health threat.”
The term “new” does not necessarily refer to new inventions — several NPS were first synthesized
decades ago — but to substances that have recently become available on the market.
Examples of NPS are:
Natural origin NPS
Kratom/ Ketum
Khat/ Bushman’s tea
Salvia/ Salvia divinorum
Magic Mushrooms/ Psilocybe Cubensis
Mandrake
New Psychoactive Substances (Other name)
Synthetic drugs Plant fertiliser
Legal high Herbal incense
Herbal highs Room deodorisers
Party pills Aphrodisiac tea
Synthetic cocaine Social tonics
Synthetic cannabis New and emerging drugs (NEDs)
Herbal ecstasy Drug analogues
NBOMes Research chemicals.
Bath salts
NPS by group effects

Synthetic carnabinnoid
Synthetic opioids
Classic hallucinogens
Stimulants
Sedatives/Hypnotics
Substance-induced
Psychotic Disorder
 CLINICAL FEATURE
Early warning signs that may indicate episode of psychotic behaviour:
Significant decline in work or school performance
Social withdrawal or isolation
Neglect hygiene and personal care
Decline in ability to concentrate or complete simple tasks
Loss of ability to communicate effectively
Sudden bouts of paranoia, mistrust or unprovoked hostility
Intense emotional outbursts or a complete lack of emotional expression
Strange behaviours or statements that might indicate the presence of
delusions or mild hallucinations
CLINICAL FEATURE
Symptoms that is shown in full-blown substance-induced psychotic
disorder:
Hallucinations
Delusions
Hostility, aggressiveness, suspicion
Complete inability to manage daily tasks or handle personal
responsibilities
Extreme, persistent anxiety
Disruptions in sleeping and eating
Depression or other signs of mood disorders
DELUSIONS
Secondary and substance-induced delusions are usually present in a
state of full wakefulness
Patients experience no change in the level of consciousness although
mild cognitive impairment may be observed
Patients may appear confused, disheveled or eccentric with tangential
or even incoherent speech
Hyperactivity and apathy may be present and an associated dysphoric
mood is thought to be common
The delusions can be systematized or fragmentary with varying content
but persecutory delusions are the most common
HALLUCINATIONS
Can occur in one or more sensory modalities
Are either recurrent or persistent and are experienced in a state of full
wakefulness and alertness
Patient shows no significant changes in cognitive functions
DSM-5 Diagnostic Criteria
A Presence of one or both of the following symptoms:
1. Delusions
2. Hallucinations

B There is evidence from the history, physical examination, or laboratory findings of both (1)
and (2):
1. The symptoms in Criterion A developed during or soon after substance intoxication or
withdrawal or after exposure to a medication
2. The involved substance/medication is capable of producing the symptoms in Criterion A

C The disturbance is not better explained by a psychotic disorder that is not

substance/medication-induced. Such evidence of an independent psychotic disorder
could include the following:
1. The symptoms preceded the onset of the substance/medication use
2. The symptoms persist for a substantial period of time (e.g., about 1 month) after the
cessation of acute withdrawal or severe intoxication
3. Or there is other evidence of an independent non-substance/medication-induced
psychotic disorder (e.g., a history of recurrent non-substance/medication-related
episodes)
D The disturbance does not occur exclusively during the course of delirium

E The disturbance causes clinically significant distress or impairment in social,

occupational, or other important areas of functioning

NOTE: The diagnosis should be made instead of a diagnosis of substance intoxication or

substance withdrawal only when the symptoms in Criterion A predominate in the clinical
picture and when they are sufficiently severe to warrant clinical attention
 CAUSATIVE AGENTS

Diagnostic and Statistical Manual of Mental Disorders 5th edition

 PRINCIPLE OF MANAGEMENT
1. Pharmacological intervention
antipsychotics

2. Physical intervention
Electroconvulsive therapy: need for rapid improvement, reduction of symptom & limited
response to antipsychotics

3. Psychological intervention
Psychoeducation: diagnosis, psychosocial intervention, medication & side effects, stress &
coping, early warning sign, suicide & relapse prevention
Cognitive behaviour therapy

4. Social intervention
Rehabilitation
Family therapy
Community psychiatric service

Management of schizophrenia 2nd edition

 BRIEF INTERVENTION FOR
SUBSTANCES USE
AIM:
to identify current or potential problems with substance use and motivate
those at risk to change their substance use behaviour.
to encourage those with serious dependence to accept more intensive
treatment.
to help patient to understand the substance is putting them at risk
to encourage people to reduce or give up their substance use.
 BRIEF INTERVENTION FOR SUBSTANCES USE
COMPONENTS: FRAME
Give relevant feedback based on information about the individual’s drug use and related
1. Feedback
problems from screening instrument.

Acknowledge that they are responsible for their own behaviour.

2. Responsibility
ex: What you do with your substance use is up to you”

3. Advice Provide clear advice regarding the harms associated with continued use.

Provide the patient with a range of alternative strategies to cut down or stop their
4. Menu of option
substance use.

5. Empathy Use warm, reflective, empathic and understanding approach

Encourage patient’s confidence that they are able to make changes in their substance use
6. Self efficacy
behaviour.
Thank you!
PETER WONG QIN CHAI
MOA of alcohol, types of alcohol, alcohol unit consumption formula
MARIE ISABEL ANAK NANANG
Complications & investigations of alcohol misuse, alcohol intoxication & withdrawal
STEFANIE BACHA ANAK MENARI
Delirium tremens, biopsychosocial management of alcohol use disorders
NURUL AKMA AZWA AZ ZAHRA BINTI RAMLI
Types, MOA, route of administration, intoxication & withdrawal features, investigations, management of
opioids-, hallucinogens- & stimulants-use disorder
MUHAMMAD HARITH BIN NOORDDIN
Types, MOA, route of administration, intoxication & withdrawal features, investigations, management of
sedatives-/ hypnotics-/ anxiolytics-, caffeine- & tobacco-use disorder
AIRUL SHAMIRZUAN BIN MOHAMAD SAFRI
Types, MOA, route of administration, intoxication & withdrawal features, investigations, management of
cannabis-, inhalants- & new psychoactive substances-use disorder
RESHME ASHWHINI A/P RAJASEGAR
Clinical features, diagnosis of substance-induced psychotic disorder
NUR IZZ SABRINA BINTI OTHMAN
Causative agents & management of substance-induced psychotic disorder, brief intervention for substances
use
 References
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