GC166 I Cannot Help Myself, Taking These Pills Just Feels Good Substance Abuse And Addiction
Substance abuse and addiction is a chronic relapsing disorder characterized by compulsive drug seeking, continued use despite harmful consequences, and long-lasting neuroplastic changes in brain reward, motivation, and self-control circuits.
Substance Use and Addiction
This lecture (GC 166) by Dr. Sherry K.W. Chan covers the entire spectrum of substance abuse and addiction — from definitions and terminology, through the neurobiology of why people become addicted, to clinical assessment, diagnosis, impact, and the stages-of-change model that underpins treatment planning. The lecture is deliberately mechanistic: it wants you to understand why addiction happens at the level of brain circuits before you try to assess or manage a patient.
Learning Objectives (from slide outline):
- Define key terminology: problem use/misuse, craving, dependence, addiction
- Understand the biological basis of addiction (reward pathway, tolerance, withdrawal, craving)
- Approach assessment and diagnosis of substance use disorders
"Addiction is an attachment to, or dependence upon, any substance, thing, person or idea so single-minded and intense that virtually all other realities are ignored or given second place — and consequences, even lethal ones, are disregarded" — John F. Mack (2002) [3]
This quote frames the entire lecture: addiction is not just about drugs. It is a pattern of behaviour where the reinforcing stimulus overrides all other drives.
| Term | Lecture wording | Current clinical interpretation |
|---|---|---|
| Problem Use / Misuse | Use for pleasure but with disregard for personal or social dangers | Describes risky or harmful use, but is not necessarily an early linear stage and does not establish whether control is lost |
| Craving | Strong and sometimes irresistible desire to use; not necessarily pleasurable | Key distinction: craving is about compulsion, not enjoyment. It can be triggered by cues or stress even long after withdrawal resolves. |
| Physical dependence | Physiological adaptation → withdrawal when exposure is abruptly reduced | Can occur during appropriate prescribed treatment and is not the same as addiction [10] |
| Psychological dependence | Psychological withdrawal symptoms such as anxiety, dysphoria or insomnia | A historical mind/body split; symptoms are biologically real, but modern diagnosis assesses the integrated cognitive, behavioural and physiological syndrome |
| Addiction / substance use disorder | Lecture: extreme end of a dependent spectrum with social/personal decline | Clinically, impaired control and compulsive use despite harm are central. Tolerance and withdrawal may occur but are neither necessary nor sufficient on their own [10] |
Terminology has moved on
The slides teach ICD-10 dependence syndrome and use “drug abuser/addict,” so know those labels for the lecture. In clinical writing, prefer person-first language (“person with a substance use disorder”). ICD-11 separates hazardous use, harmful patterns and dependence and simplifies its dependence guidance; do not silently apply the ICD-10 “3 of 6” rule when a question explicitly asks for ICD-11. [11]
Exam Trap: Craving ≠ Pleasure
Students often assume craving = wanting the pleasurable high. The lecture explicitly states craving is "not necessarily pleasurable" — it is a compulsive drive to use, often driven by negative reinforcement (avoidance of withdrawal distress) or conditioned cues, not the pursuit of euphoria. This distinction is a favourite MCQ discriminator.
ICD-10 requires ≥3 of the following 6 criteria to be present together at some time during the previous year: [3][4]
This threshold is correct for the ICD-10 slide/exam framework. It is not a screening cut-off: establish the substance, time course, impairment, risk and differential diagnosis rather than diagnosing from tolerance or a positive toxicology result alone.
| # | Criterion | First-Principles Explanation |
|---|---|---|
| a | Strong desire or sense of compulsion to take the substance | The subjective craving — this is the psychological drive. |
| b | Difficulties in controlling substance-taking behaviour (onset, termination, or levels) | Loss of volitional control — they can't stop when they want to, can't limit how much they use. |
| c | Physiological withdrawal state when use has ceased or been reduced | The body fights back when the drug is removed — neuroadaptation unmasked. |
| d | Evidence of tolerance | Need more drug for the same effect — receptor downregulation. |
| e | Progressive neglect of alternative pleasures or interests | The drug reinforcer supersedes natural reinforcers (food, sex, work, hygiene). |
| f | Persisting with substance use despite clear evidence of overtly harmful consequences | Continued use despite knowing it causes harm — the hallmark of loss of insight/control. |
High Yield: ICD-10 Dependence Mnemonic
CANT Control Withdrawal [4]:
- Compulsion to use substance
- Aware of harm but continues
- Neglect of alternative activities
- Tolerance
- Can't CONTROL substance use behaviour
- WITHDRAWAL state
The lecture lists the following categories of substances: [3]
| Category | Examples | Notes |
|---|---|---|
| Alcohol | — | Most common substance of abuse globally; covered in detail in GC 161 |
| Opioids | Heroin, morphine, codeine, methadone | Separate intoxication/overdose, withdrawal, prescribed physical dependence and opioid use disorder. Methadone may be a drug of misuse or prescribed treatment; the clinical context matters. |
| Cocaine | Cocaine, crack | Stimulant; potent DA reuptake inhibitor |
| Amphetamines | Methamphetamine ("ice") | Stimulant intoxication can cause agitation, hyperthermia, cardiovascular toxicity and psychosis |
| Sedatives, hypnotics, anxiolytics | Benzodiazepines, Z-drugs | Physical dependence and withdrawal can develop during prescribing; avoid routine long-term use and taper rather than abruptly stopping a dependent patient [1] |
| Hallucinogens / entactogens | LSD; MDMA (“ecstasy”) is better described as an entactogen-stimulant with perceptual effects | MDMA is predominantly monoaminergic and can contribute to hyperthermia, hyponatraemia and serotonin toxicity |
| Dissociatives | PCP, ketamine | NMDA-receptor antagonism; ketamine can cause dissociation and, with chronic heavy exposure, urinary-tract injury |
| Inhalants | Glue, solvents | Typically adolescents; can cause sudden cardiac death |
| Cannabis | Marijuana | Endocannabinoid system; CB1 receptor |
| Nicotine | Cigarettes | Most prevalent substance dependence globally |
| Caffeine | Coffee, tea, energy drinks | Often overlooked; genuine withdrawal syndrome exists |
Methadone treatment is not evidence of misuse
Methadone and buprenorphine are evidence-based medications for opioid use disorder. Do not label a person as “addicted” merely because they receive agonist treatment or develop expected physical dependence. Clarify the indication, prescription and use pattern; avoid abrupt unsupervised cessation.[10][14]
Reading the historical Hong Kong trend charts
Slides 6–7 contain four Central Registry of Drug Abuse (CRDA) line charts: all ages and aged under 21, each shown in two historical windows (first half-years, 2015–2018; and first three quarters, 2019–2022).
All ages (slide 6)
- Heroin is the highest single line in both panels but trends downward overall. “Ice” rises then falls in the earlier panel and continues downward in the later panel.
- Cocaine rises into 2021 before falling in 2022 in the later window; cannabis, ketamine and tranquilizer/hypnotic lines are lower in these particular panels.
Aged under 21 (slide 7)
- In the earlier panel, the “ice” line falls markedly while cocaine rises by the right-hand end; heroin stays comparatively low.
- In the later panel, cannabis and cocaine are the dominant reported lines, with a conspicuous late rise in ketamine; “ice” and MDMA plot lower.
How to interpret the figures
- These are reported-person counts, not population prevalence. The CRDA itself cautions that its statistics do not measure the exact size of Hong Kong's drug-using population; they are indicators of trends among people known to the reporting system.[13]
- A person using several drugs may appear in more than one drug category, and reporting coverage can change.
- The windows and axes differ, so compare direction and relative pattern within each panel rather than absolute heights across panels. Treat the 2015–2022 graphics as historical lecture context and use current CRDA tables for present-day patterns.[13]
4. Biological Basis of Addiction — The Core Neuroscience
This is the heart of the lecture. The lecturer builds the model in stages, adding brain circuits for each stage of addiction.
A reinforcer increases the likelihood of a behaviour that precedes its presentation. [3]
| Type | Definition | Role in Addiction |
|---|---|---|
| Positive reinforcement | A positive/pleasurable outcome follows the behaviour | Early stage: drug use → euphoria → repeat use. "Impulsive act" with increased arousal/tension before the act. |
| Negative reinforcement | Behaviour is supported by avoidance or termination of aversive events | Later stage: drug use → relief from withdrawal anxiety/stress → compulsive use. |
The diagram's central transition is from predominantly positive reinforcement/impulsive use toward negative reinforcement/compulsive use. [3] This is a useful model, not an inevitable sequence: motives can coexist, trajectories differ by substance and person, and repeated use does not automatically become addiction.
- Impulsive act: Increased sense of arousal and tension before the act → positive reinforcement (the high)
- Compulsive act: Anxiety and stress before → relief after → negative reinforcement (escaping withdrawal)
This explains one mechanism sustaining use after pleasure has diminished: taking the substance can rapidly remove an aversive withdrawal or negative-affect state.
Lecture classification: [3]
| Category | Neurotransmitters | Role |
|---|---|---|
| “Primary” in the slide | Glutamate (predominantly excitatory), GABA (predominantly inhibitory) | Fast synaptic signalling, plasticity, learning and memory |
| “Secondary/modulatory” in the slide | Dopamine, noradrenaline, acetylcholine, endogenous opioids, endocannabinoids, serotonin | Modulate circuit state, salience, stress, arousal and reinforcement |
The primary/secondary split is the lecturer's teaching scaffold, not a standard formal neurotransmitter taxonomy. A transmitter's effect depends on receptor subtype, circuit and location; “glutamate = positive” and “GABA = negative” mean excitatory/inhibitory tendencies, not good/bad psychological effects.
Endogenous 'addictive' neurotransmitters: [3]
- Opioid peptides (e.g., endorphins) — endogenous ligands at opioid receptors
- Endocannabinoids (e.g., anandamide) — endogenous ligands in the cannabinoid system
All drugs of abuse interact with neurotransmitters by one of three mechanisms: [3]
- Mimic natural transmitters (e.g., morphine mimics endorphins at opioid receptors)
- Release transmitters (e.g., amphetamines cause massive dopamine release)
- Block a receptor, transporter or enzyme (e.g., cocaine blocks monoamine reuptake transporters)
4.3 The Three-Stage Addiction Cycle
The lecture progressively builds a three-stage cycle, adding neuroanatomy at each stage:
The mesolimbic dopamine system is the reward pathway. Drugs of abuse increase dopamine (DA) in the nucleus accumbens. Activation produces positive reinforcement effects. [3]
Key structures:
- Ventral Tegmental Area (VTA): Origin of the mesolimbic dopamine pathway
- Nucleus Accumbens (NAcc): A ventral-striatal hub receiving VTA dopamine and integrating salience, action and reinforcement signals; it is not a single anatomical “pleasure centre”
- Amygdala: Emotional salience / association of cues with reward
- Hippocampus: Contextual memory of drug-taking situations
The slide states that all drugs of abuse activate the mesolimbic dopamine system and gives cannabinoid/opioid examples of indirect reinforcement at NAcc. [3]
Use that as the lecture's common-final-pathway model rather than a literal single-mechanism rule. Substance classes act first at different receptors and circuits, and dopamine is especially important for incentive salience, prediction/learning and motivated action—not simply “pleasure.”
When the reinforcers are too powerful, natural drives (sex, work, eating, hygiene) may be subsumed and ignored. [3]
This explains criterion (e) of the ICD-10: progressive neglect of alternative pleasures — the drug hijacks the reward system so completely that natural rewards cannot compete.
Tolerance:
Neuroplasticity: Adaptations in receptors and post-receptor mechanisms (e.g., change the number of receptors) → Tolerance [3]
- Repeated exposure can alter receptor number, intracellular signalling, gene expression and circuit connectivity; tolerance is substance- and effect-specific.
- The slide's PET montage (Volkow et al., 1999) shows lower striatal D2/D3 receptor availability in groups using cocaine, methamphetamine or alcohol than in comparison groups. In the colour scale, warmer red/yellow signal means greater measured availability; the substance-use images are cooler/dimmer.
- This is a group association, not a diagnostic scan and not proof that low D2 availability alone caused the disorder or directly explains every form of tolerance. Exposure, recovery duration and pre-existing vulnerability may all contribute.
Withdrawal:
Activation of the extended amygdala. Major neurotransmitters involved are corticotropin-releasing factor (CRF) and norepinephrine. Major projection to hypothalamus and brainstem. [3]
Why these transmitters in the slide model?
- CRF and noradrenergic signalling contribute to stress/negative-affect circuitry in the extended amygdala.
- Hypothalamic and brainstem projections connect this state to endocrine and autonomic responses.
- The actual withdrawal phenotype is drug-specific: autonomic overactivity is prominent with alcohol/opioids, whereas stimulant withdrawal more often features fatigue, sleep/appetite change and dysphoria.
The withdrawal state provides powerful negative reinforcement: use the drug again → CRF/NE activity drops → relief.
Craving is the key element of relapse in humans, driven by: [3] a) Drug seeking induced by drug or stimuli paired (cue) with drug taking b) Drug seeking induced by an acute stressor or a residual negative emotional state (protracted abstinence)
Neural circuitry of craving:
| Structure | Function in Craving |
|---|---|
| Amygdala | Conditional reinforcement — associates environmental cues (people, places, paraphernalia) with the drug reward |
| Hippocampus | Contextual information processing — remembers where, when, and how drugs were obtained |
| Prefrontal cortex | Executive control and action selection; top-down regulation may be weakened in established substance use disorder |
| Major transmitter: Glutamate | The excitatory drive behind craving — glutamatergic projections from PFC to NAcc |
The full addiction cycle involves: [3]
- Impulsivity (driven by VTA-NAcc reward circuit, modulated by frontal cortex top-down control)
- Compulsivity (driven by anterior cingulate, prefrontal cortex, amygdala, hippocampus)
- Failed top-down control (frontal cortex dysfunction allows impulsivity and compulsivity to dominate)
High Yield: Complete Stage Model with Brain Regions
| Stage | Behaviour | Brain Region | Neurotransmitter | Reinforcement Type |
|---|---|---|---|---|
| Binge/Intoxication | Drug use for pleasure | VTA → Nucleus Accumbens | Dopamine | Positive |
| Withdrawal/Negative Affect | Dysphoria, stress and drug-specific withdrawal; tolerance may have developed | Extended amygdala with hypothalamic/brainstem outputs | CRF/NE stress signalling in the model; multiple substance-specific systems | Negative |
| Craving/Preoccupation | Cue-triggered/stress-triggered drug seeking | Amygdala, Hippocampus, Prefrontal cortex, Orbitofrontal cortex | Glutamate | Conditioned / Habitual |
The lecturer reuses the same circular figure and adds one layer at a time:
- Base loop: binge/intoxication → withdrawal → craving/preoccupation → renewed binge. The arrows mean feedback, not three isolated boxes.
- Red overlay: VTA–NAcc reward circuitry is recruited during intoxication and drug reinforcement.
- Blue overlay: after tolerance develops, withdrawal/negative affect recruits anterior cingulate, prefrontal and amygdala-related circuitry.
- Green overlay: hippocampal context memory and amygdala-conditioned cues feed craving; prefrontal/orbitofrontal systems evaluate and select action.
- Final downward arrow: weakened frontal top-down control allows impulsive responding to become increasingly compulsive.
The last image therefore explains relapse as a competition between cue/stress-driven bottom-up signals and executive control—not as a moral failure.
Personality is controversial, but: [3]
- Sensation-seeking, impulsive, extrovert personality traits → predispose to experimentation with drugs
- Obsessional, dependent, anxious personality traits → more likely to become dependent and find it difficult to stop
These are probabilistic trait associations from the lecture, not “addictive personalities.” They must not be used to blame a patient or predict an individual's outcome; trauma, psychiatric symptoms, drug availability, social determinants, genetics and protective factors interact.
Environment affects dopamine systems: Morgan et al. (2002) [3]
- Monkeys that became dominant after social housing showed higher striatal D2 receptor availability than when individually housed
- This was associated with less cocaine self-administration than in subordinate animals
Reading the four PET panels: compare each row across columns. The dominant animal's socially housed scan becomes much brighter, whereas the subordinate animal shows little comparable change. This supports an environment-sensitive association between social position, D2 availability and cocaine reinforcement. It does not directly test genes, prove a simple “social enrichment protects” pathway, or justify extrapolating dominance effects one-to-one from monkeys to an individual patient.
5. Assessment and Diagnosis
Three aims: [3]
- Differentiating the drug-using problem — making a diagnosis
- Formulation: What, Why, How
- Understand the problems/difficulties
- Understand the needs
- Understand the person
- Facilitating establishment of treatment plan — requires knowing the patient's stage of change
Turning “What, Why, How” into a usable history
| Domain | Ask explicitly |
|---|---|
| What | Every substance including alcohol, nicotine, prescribed/over-the-counter drugs; formulation, amount, frequency, duration, last use, binges, mixing, intoxication, withdrawal, craving, loss of control, tolerance, overdoses and previous treatment |
| Why / when | Desired effect, symptoms relieved, triggers, cues, stress, pain/sleep/trauma, social context, changing motives, what the patient values and wants help with |
| How | Route, source, setting/solitary use, injecting or smoking equipment, sharing, money/legal exposure, driving/sex/violence risk and access to emergency help |
| Impact | Physical and mental health, suicide/self-harm risk, cognition, relationships, caring responsibilities, housing, study/work, finance and justice involvement |
| Protection and need | Coping skills, family/peer support, treatment preferences, pregnancy, infection/vaccination needs, naloxone, withdrawal risk and immediate safeguarding |
Quantify in the patient's own units first, then convert where meaningful. Ask non-judgmentally and explain confidentiality limits; people disclose more accurately when the purpose is safety rather than punishment.
Diagnosis is based on: [3]
- Diagnostic criteria (ICD-10 as above): tolerance, withdrawal, compulsion
- Drug screening/testing: urine toxicology, blood tests
- Screening tools: e.g., CAGE questionnaire for alcohol misuse
Toxicology is supportive, not diagnostic. Interpret the specimen, detection window, cross-reactivity and substances omitted from the panel. A positive result does not prove intoxication, impairment or a substance use disorder; a negative result does not exclude one. Obtain consent and use results to improve safety and treatment rather than punish disclosure.
CAGE — An Alcoholism Screening Test: [3]
- 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 — Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover? (Eye-opener)
Two positive responses = positive test → further assessment warranted (Ewing, 1984) [3]
How to use CAGE
CAGE is a brief screen, not a diagnosis or measure of current consumption. Two positive answers in the lecture's scoring rule warrant a fuller alcohol history and validated diagnostic assessment. An eye-opener may suggest relief of morning withdrawal, but no single answer proves physical dependence; wording such as “alcoholism test” is historical.
Understanding why is an important part of assessment because it leads to effective treatment. [3]
The slide poses “pleasure seeking?” beside “20%” and stresses that reasons are dynamic. [3]
Treat the 20% as a dated teaching prompt linked to a 1994 college-alcohol list, not a universal prevalence estimate for all people, substances or settings. The durable lesson is to ask the patient what the substance does for them now, because functions and motives change.
Top 10 reasons college students give for consuming alcohol (Adler & Rosenberg, 1994) [3]:
- Increase feelings of sociability
- Relieve anxiety or tension
- Feeling elated/euphoria
- Less inhibited
- Go along with friends (peer pressure)
- Experience different state of consciousness
- Less inhibited sexually
- Stop worrying
- Alleviate depression
- Less self-conscious
Broader reasons for drug use (lecture summary) [3]:
- High and buzz (pleasure-seeking)
- Self-medication for anxiety, social anxiety, anger, pain, boredom, lack of confidence/motivation
- Psychiatric problems: depression, drug side effects, anxiety-related problems
- Social pressure: peer effect, life events, adversity
- Search for meaning or mystical experiences
Clinical Pearl: ask what problem the substance solves
Substance use may regulate anxiety, trauma symptoms, pain, insomnia, loneliness or social belonging, but “self-medication” is a hypothesis to explore rather than assume. Assess comorbidity and treat both conditions; avoid causal claims from temporal overlap and avoid telling a patient relapse is inevitable.
5.5 Impact of Addiction — The "What"
Faster the drug reaches the target site in the brain, the better they are liked and more psychologically reinforcing. [3]
This is a pharmacokinetic principle, not a complete safety ranking: rate of concentration rise generally strengthens reinforcement, but dose, formulation, half-life, contaminants, co-use and host factors also determine harm.
| Route of Administration | Speed to Brain | Implication |
|---|---|---|
| Ingestion (oral) | Usually slower onset than inhaled/IV delivery | Slower rise often reduces immediate reinforcement, but oral overdose and organ toxicity can still be fatal |
| Inhalation / smoking | Rapid pulmonary absorption | Rapid concentration change can strengthen reinforcement; also adds pulmonary/thermal harms depending on product |
| Injection (SC, IM, IV) | IV gives immediate bioavailability; SC/IM kinetics vary | Adds bloodstream infection, blood-borne virus, tissue injury and overdose risk; route alone does not determine the whole risk profile |
Other medical impacts [3]:
- Form/substances: state of intoxication/withdrawal (each substance has characteristic syndromes)
- Chronic use: organ damage (liver, brain, lungs, heart, kidneys)
- Self-care: neglect of nutrition, hygiene, medical follow-up
Comorbid mental health problems: [3]
- Anxiety
- Depression
- Psychosis (substance-induced)
- Motivational problems
- Insomnia
[3]:
- Relationship breakdown
- Housing instability/homelessness
- Vocational loss
- Financial problems
- Criminal activity
Assess: [3]
- Personality
- Resources
- Coping methods
- Support network
- Other problems
- Subjective understanding, views, and needs — what does the patient think is happening? What do they want?
Needs are tripartite: [3]
- Medical needs (detoxification, treatment of complications, comorbidities)
- Psychological needs (therapy for underlying conditions, coping skills)
- Social needs (housing, employment, legal issues, family support)
This model is essential for treatment planning — you cannot effectively treat someone who isn't ready to change. [3]
Use the model to match the conversation, not to withhold care. Even someone not pursuing abstinence can benefit from overdose prevention, safer-use advice, treatment of comorbidity, vaccination/testing, naloxone and a non-judgmental invitation to return.
| Stage | Analogy (Lecture) | Description | Clinical Approach |
|---|---|---|---|
| Pre-contemplation | "Ignorance is the bliss" | Not aware of / not acknowledging the problem | Raise awareness; provide information; don't push |
| Contemplation | "Sitting on the fence" | Aware of problem, ambivalent about change | Motivational interviewing; explore pros/cons |
| Preparation | "Testing the water" | Intending to take action, making small steps | Help plan concrete steps; set goals |
| Action | — | Actively modifying behaviour | Support change; provide resources; pharmacotherapy if needed |
| Maintenance | — | Sustained change; preventing relapse | Ongoing support; relapse prevention strategies |
| Relapse / return to use | Slide: “Fall from grace” | Return after a period of change; may be brief or sustained | Assess overdose risk and loss of tolerance, learn from triggers, re-engage care; avoid moralising language |
High Yield: Stages of Change Are Cyclical, Not Linear
The lecture image is circular: every arrow points onward and “relapse” feeds back rather than ending the process. People can move in either direction, skip stages or pursue goals other than abstinence, so the model is a conversational aid rather than a diagnostic law.
This is directly tested in past papers (see below). The 2022 item uses a classic exam clue:
Visual hallucinations are more suggestive of substance-induced psychosis than schizophrenia. [5]
That is a likelihood clue, not a diagnostic discriminator. Visual hallucinations occur in primary psychotic disorders too, while stimulant-induced psychosis can be predominantly auditory. Diagnosis requires a plausible substance, a close temporal relationship to intoxication/withdrawal, evidence from history/collateral/toxicology when appropriate, and exclusion of delirium and an independent primary disorder.
| Feature | Substance-Induced Psychosis | Primary Psychosis (Schizophrenia) |
|---|---|---|
| Visual hallucinations | May be prominent in toxic/organic states; an exam pointer | Can occur; auditory hallucinations are more typical but not exclusive |
| Auditory hallucinations | Can occur | Hallmark feature |
| Persecutory delusions | Can occur in both | Can occur in both |
| Passivity experience | Less typical | More specific to schizophrenia |
| Disorganised speech | Can occur in both | Can occur in both |
| Temporal relationship | Develops during or soon after exposure/withdrawal and fits the pharmacology | Symptoms precede exposure, recur during sustained abstinence or have an independent course |
| Course | Often improves as the drug state clears, but stimulant psychosis can persist or recur | Persistent/recurrent course independent of substance state |
| Other clues | Autonomic/toxic signs, fluctuating attention or altered consciousness suggest intoxication or delirium, not uncomplicated psychosis | Prodrome, negative symptoms, thought disorder and family history may support a primary disorder but are not decisive alone |
Safety before labels
Agitation or psychosis after substance use still requires ABCs, temperature, glucose, ECG when indicated, assessment for delirium/head injury/infection and risk to self or others. Do not postpone treatment while arguing whether the final label is “substance-induced” or “primary.”
From the 2023 MCQ Q74 [6], a classic clinical scenario:
Clinical features of opioid overdose:
- Slow, shallow or absent breathing is the life-threatening feature; snoring/gurgling in an unrousable patient can be airway obstruction, not normal sleep
- Reduced consciousness or inability to wake
- Pinpoint pupils support the diagnosis but may be absent with hypoxia, co-ingestion or some opioids
- Cyanosis/low oxygen saturation, hypotension or bradycardia in severe poisoning
- Drug paraphernalia or injection scars may support exposure but are neither necessary nor specific
Management:
- Call for emergency/resuscitation help. Open the airway and support oxygenation and ventilation immediately; use bag-mask ventilation/CPR according to pulse and breathing rather than waiting for an antidote.
- Give naloxone promptly. In clinical care, titrate to adequate spontaneous ventilation rather than demanding full wakefulness; community formulations follow their labelled dose. Repeat after 2–3 minutes if breathing has not recovered. [12]
- Reassess ABCs, glucose, temperature and possible co-ingestants/trauma. Naloxone's effect may wear off before the opioid, so recurrent respiratory depression may require repeat dosing/infusion and monitored observation.
- If chronic opioid exposure is likely, an abrupt large antagonist dose may precipitate severe withdrawal—but this never justifies withholding naloxone from life-threatening respiratory depression.
For the MCQ, naloxone is the best listed answer. Flumazenil is not routine empirical coma treatment because chronic benzodiazepine use or mixed overdose can make it hazardous; dextrose treats hypoglycaemia, and thiamine treats/prevents Wernicke encephalopathy but neither reverses opioid hypoventilation.
9. Integration with Related Lectures
- Alcohol dependence is covered in detail in GC 161; the CAGE questionnaire from GC 166 directly applies
- Delirium tremens = severe alcohol withdrawal with delirium plus autonomic hyperactivity; withdrawal seizures can occur before it and do not by themselves define DT
- Management is monitored, symptom-triggered or protocol-based benzodiazepine therapy plus fluids/electrolyte and complication care; give thiamine to at-risk patients. Do not delay emergency glucose for hypoglycaemia while waiting for thiamine
- Substance misuse is a mandatory enquiry in psychiatric history-taking, specifically under HPI risk assessment and premorbid personality [2]
- Always ask about: type of substance, route, frequency, quantity, last use, withdrawal symptoms, previous treatment, forensic history
- Benzodiazepines and Z-drugs are usually poor default long-term treatments because of tolerance, dependence, falls/cognitive effects and interaction risk; selected exceptions require a documented indication and review [1]
- Long-term management options include antidepressants, antipsychotics, mood stabilizers
- Addiction (including non-substance, e.g., gambling) and impulse-control disorders (e.g., trichotillomania) are classified under "impaired behaviours" [7]
10. Exam Intelligence
- Differentiate delirium from delirium tremens — tested in AOS MCQs [1]
- Alcohol withdrawal management (complications: seizures) [1]
- Medication questions: dependence risks of benzodiazepines/Z-drugs and why they are poor routine long-term choices [1]
- Substance-induced psychosis vs. schizophrenia — visual hallucinations are the cited MCQ clue, but not a stand-alone clinical discriminator [5]
- Opioid overdose management — naloxone [6]
- CAGE questionnaire — know all 4 questions and the cut-off (≥2 positive)
- ICD-10 dependence criteria — know all 6 and the threshold (≥3)
| Trap | Correct Understanding |
|---|---|
| "Craving means wanting the pleasure again" | Craving is not necessarily pleasurable — it is compulsive and can be driven by negative reinforcement |
| "Addiction = physical dependence" | Physical dependence can arise during correct treatment. Addiction centres on impaired control/compulsive use despite harm; tolerance and withdrawal are neither necessary nor sufficient |
| "Every drug is just a dopamine drug" | The slide uses mesolimbic dopamine as a common reinforcement model, but each class has distinct primary targets and non-dopaminergic circuits |
| "Low D2 PET signal proves addiction or caused it" | It is a group association affected by exposure, recovery and vulnerability; PET is not a diagnostic test |
| "Tolerance = one universal receptor downregulation" | Tolerance is effect- and substance-specific and may reflect receptor, post-receptor, metabolic, behavioural and contextual adaptation |
| "There is an addictive personality" | The slide's trait associations are probabilistic and controversial; never use them as deterministic labels |
| "Relapse = treatment failure" | Return to use is information for risk assessment and plan revision; urgently address lost tolerance and overdose risk |
High Yield Summary
-
Terminology hierarchy
- Do not force a hierarchy. Physical dependence can occur without addiction; addiction/SUD centres on impaired control and continued use despite harm. Craving is not necessarily pleasurable.
-
ICD-10 Dependence = ≥3 of 6 criteria
- (CANT Control Withdrawal): Compulsion, Aware of harm, Neglect of alternatives, Tolerance, Can't Control, Withdrawal.
-
Three-stage addiction cycle
- Binge/intoxication (VTA–NAcc reinforcement) → withdrawal/negative affect (extended-amygdala stress systems) → preoccupation/anticipation (cue/context memory plus executive control) → renewed use.
- Tolerance is an adaptation, not the formal name of the second stage; weakened top-down control and strengthened cue/stress responses perpetuate the loop.
-
How to read the D2 PET montage
- Substance-use groups show lower striatal D2/D3 availability than comparison groups. It is an association, not a diagnostic scan or proof of a single causal pathway.
-
The dopamine pathway is a teaching model
- VTA–NAcc dopamine helps reinforcement/salience learning, but substances have distinct primary molecular targets and additional circuits.
-
CAGE questionnaire
- Cut down, Annoyed, Guilty, Eye-opener. ≥2 positive = further assessment warranted.
-
Why people use drugs matters for treatment
- Reasons are dynamic: reward, relief, belonging, symptoms and context may coexist. The slide's “20%” is a dated prompt, not a universal prevalence estimate.
-
Route matters
- A faster brain concentration rise often increases reinforcement, but route does not create a universal safety ranking; dose, formulation, co-use and context matter.
-
Prochaska & DiClemente Stages of Change
- Pre-contemplation → Contemplation → Preparation → Action → Maintenance → Relapse (cyclical, not linear).
-
Substance-induced psychosis
- Visual hallucinations are a past-paper clue, not diagnostic. Establish temporal/pharmacological plausibility and exclude delirium and an independent primary psychosis.
- Opioid overdose triad
- Reduced consciousness + slow/absent breathing ± miosis: support ventilation, give naloxone, repeat/reassess and monitor for recurrent toxicity.
Active Recall - Lecture Notes
[1] AOS - Psych.md [2] General Clerkship-Psychiatric Assessment Skills Training-Learning Materials 2024_3 Sep.pdf (pages 9-10, 18) [3] GC 166. I cannot help myself, taking these pills just feels good Substance abuse and addiction.pdf (pages 1-40) [4] Ryan Ho Psychiatry.pdf (pages 112-113) [5] 2022 Fourth Summative MCQ.pdf (Q26, page 10) [6] 2023 Fourth Summative MCQ.pdf (Q74, page 28) [7] CFB (PSY02) Classification and Diagnosis of Psychiatric Illness.pdf (page 18) [8] 2020 Fourth Summative Assessment MCQ paper.pdf (pages 41-42) [9] 2017 Fourth Summative SAQ.pdf (Q11, page 5) [10] National Institute on Drug Abuse. Misuse of Prescription Drugs Research Report: Understanding Dependence, Addiction, and Tolerance. https://nida.nih.gov/sites/default/files/2609-misuse-of-prescription-drugs.pdf [11] World Health Organization. Alcohol, Drugs and Addictive Behaviours: ICD-10 and ICD-11 terminology and categories. https://www.who.int/teams/mental-health-and-substance-use/alcohol-drugs-and-addictive-behaviours/terminology [12] US Centers for Disease Control and Prevention. What to Do If You Think Someone Is Overdosing. Updated 2024. https://www.cdc.gov/stop-overdose/response/index.html [13] Hong Kong Security Bureau, Narcotics Division. About the Central Registry of Drug Abuse and Main Charts/Tables. https://www.nd.gov.hk/en/about_crda.html; https://www.nd.gov.hk/en/crda_main_charts_and_tables.html [14] US Substance Abuse and Mental Health Services Administration. Integrating Substance Use Disorder Services into Primary and Other Care Settings. https://www.samhsa.gov/substance-use/treatment/integrating-sud-services
GC165 I Can’t Fall Asleep Sleep Physiology And Sleep Disorders
Sleep physiology encompasses the neurobiological mechanisms regulating the sleep-wake cycle, including circadian and homeostatic processes, while sleep disorders such as insomnia, narcolepsy, and obstructive sleep apnea represent disruptions in these processes leading to impaired sleep initiation, maintenance, or quality.
GC167 I Feel Very Nervous Anxiety Disorders
Anxiety disorders are a group of mental health conditions characterized by excessive, persistent fear, worry, or nervousness that causes significant distress and impairment in daily functioning.