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.
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.
How this fits into exams and clinical practice: Substance use disorders are tested both directly (MCQs on terminology, neurobiology, CAGE screening, substance-induced psychosis) and indirectly (delirium tremens, opioid overdose management, psychiatric comorbidity). The AOS intelligence confirms that "drugs-related questions usually fail" among students [1], so this is a high-discriminator topic. Substance misuse is also embedded in psychiatric history-taking as a mandatory enquiry point [2].
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 | Definition (Lecture) | Why It Matters |
|---|---|---|
| Problem Use / Misuse | Use for pleasure but with disregard for personal or social dangers | This is the earliest stage — the person hasn't lost control yet, but is ignoring consequences. Not yet dependent. |
| 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. |
| Dependence (Physical) | Physical adaptation → physical withdrawal symptoms when substance stopped | The body has adapted its neurochemistry; removing the substance unmasks the adaptation. |
| Dependence (Psychological) | Psychological withdrawal symptoms (anxiety, dysphoria, insomnia) | Mediated through the extended amygdala, CRH, and NE — not just "in their head." |
| Addiction | Extreme end of the dependent spectrum — social and personal decline, tolerance, withdrawal symptoms | The full catastrophe: tolerance + withdrawal + loss of social function. |
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]
| # | 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 | In HK, heroin historically the most common illicit drug |
| Cocaine | Cocaine, crack | Stimulant; potent DA reuptake inhibitor |
| Amphetamines | Methamphetamine ("ice") | Second most common in HK; can cause substance-induced psychosis |
| Sedatives, hypnotics, anxiolytics | Benzodiazepines, Z-drugs | Iatrogenic dependence is a major issue; BZDs not for long-term use [1] |
| Hallucinogens | LSD, ecstasy (MDMA) | Ecstasy = serotonergic; can cause serotonin syndrome |
| Phencyclidine-type | PCP, ketamine | Ketamine very relevant in HK; NMDA antagonist; causes urological damage |
| 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 |
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 transition from occasional use to addiction is the transition from positive reinforcement (impulsive act) to negative reinforcement (compulsive act). [3]
- 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 is why addiction is so hard to treat: even when the drug no longer produces euphoria (tolerance), the person keeps using because stopping causes misery.
Lecture classification: [3]
| Category | Neurotransmitters | Role |
|---|---|---|
| Primary | Glutamate (stimulatory +ve), GABA (inhibitory -ve) | Action, sensation, learning, memory |
| Secondary / Modulatory | Dopamine, Noradrenaline, Acetylcholine, Endogenous opiates, Endogenous cannabinoids, Serotonin | Modulate the primary neurotransmitter systems; these are the targets of drugs of abuse |
Endogenous 'addictive' neurotransmitters: [3]
- Opioid peptides (e.g., endorphins) — the body's own morphine
- Endogenous cannabinoids (e.g., anandamide) — the body's own cannabis
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 transmitters (e.g., cocaine blocks dopamine reuptake)
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): The "reward centre" — receives DA projections from VTA
- Amygdala: Emotional salience / association of cues with reward
- Hippocampus: Contextual memory of drug-taking situations
All drugs of abuse activate the mesolimbic dopamine system, but indirect reinforcement also occurs at the level of the nucleus accumbens — e.g., cannabinoids via CB1 receptors, opiates increase 5-HT in NAcc. [3]
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]
- Chronic stimulation of DA receptors → downregulation of D2 receptors
- Dopamine D2 receptors are persistently decreased in the brains of addicts (Volkow et al., 1999) [3]
- This means addicts need more drug to achieve the same DA effect (pharmacodynamic tolerance)
- It also means they get less pleasure from normal activities (anhedonia) — the reward threshold is raised
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?
- CRF is the stress hormone regulator — its activation during withdrawal creates intense anxiety, dysphoria
- Norepinephrine from the locus coeruleus → sympathetic overdrive (sweating, tachycardia, tremor)
- Projections to hypothalamus (HPA axis activation → cortisol) and brainstem (autonomic symptoms)
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 — should inhibit drug-seeking behaviour, but is impaired in addicts |
| 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 |
| Tolerance/Withdrawal | Need more drug; sick without it | Extended amygdala → Hypothalamus, Brainstem; Receptor downregulation | CRF, NE; ↓D2 receptors | Negative |
| Craving/Preoccupation | Cue-triggered/stress-triggered drug seeking | Amygdala, Hippocampus, Prefrontal cortex, Orbitofrontal cortex | Glutamate | Conditioned / Habitual |
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
Environment affects dopamine systems: Morgan et al. (2002) [3]
- Socially housed dominant monkeys had greater D2 receptor levels
- Associated with decreased cocaine use
- Implication: social enrichment/dominance → more D2 receptors → less vulnerability to addiction; social deprivation → fewer D2 receptors → more vulnerability
This is a beautiful example of gene-environment interaction: your social environment literally changes your receptor biology, which changes your vulnerability to addiction.
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
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
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]
Why CAGE Works
Each question targets a different dimension: Cut down = subjective awareness of problem; Annoyed = social impact; Guilty = psychological impact; Eye-opener = physical dependence (morning withdrawal requiring alcohol to relieve). Together they cover the biopsychosocial model in 4 questions.
Understanding why is an important part of assessment because it leads to effective treatment. [3]
Only ~20% take drugs purely for pleasure, and the reasons are dynamic (change over time). [3]
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: Self-Medication Hypothesis
Many patients with substance use disorders are self-medicating an undiagnosed psychiatric condition (depression, social anxiety, PTSD). Always screen for comorbid psychiatric illness. If you treat only the substance use without addressing the underlying condition, relapse is almost certain.
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]
| Route of Administration | Speed to Brain | Implication |
|---|---|---|
| Ingestion (oral) | Slowest | Least reinforcing but safest route |
| Inhalation / Smoking | Very fast (lungs → brain in seconds) | Highly reinforcing; why crack cocaine and methamphetamine are so addictive |
| Injection (SC → IM → IV) | IV = fastest | Most reinforcing; also highest risk for bloodborne infections (HIV, Hep B/C), abscesses, endocarditis |
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]
| 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 | "Fall from the grace" | Return to substance use | Normalize relapse as part of recovery; re-enter cycle; do not abandon patient |
High Yield: Stages of Change Are Cyclical, Not Linear
Patients cycle through these stages multiple times before achieving sustained recovery. Relapse is the norm, not the exception. The model teaches clinicians to match their intervention to the patient's current stage rather than forcing "action" on someone in pre-contemplation.
This is directly tested in past papers (see below). Key discriminator from the 2022 MCQ:
Visual hallucinations are more suggestive of substance-induced psychosis than schizophrenia. [5]
| Feature | Substance-Induced Psychosis | Primary Psychosis (Schizophrenia) |
|---|---|---|
| Visual hallucinations | Common — strong pointer | Less common (auditory predominate) |
| 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 | Onset during/shortly after substance use | Insidious onset independent of substance use |
| Resolution | Resolves with abstinence (usually within days–weeks) | Persistent |
From the 2023 MCQ Q74 [6], a classic clinical scenario:
Clinical features of opioid overdose:
- Pinpoint pupils (miosis) — due to opioid stimulation of Edinger-Westphal nucleus
- Respiratory depression (RR < 12)
- Decreased consciousness (GCS ↓)
- Hypotension, bradycardia
- Track marks / injection scars (groin, antecubital fossa)
Management:
- ABC + naloxone (opioid antagonist) — this is the answer to "best chance of improving mental status"
- Naloxone has shorter half-life than most opioids → may need repeated doses or infusion
- Flumazenil = benzodiazepine antagonist (wrong here)
- Dextrose = for hypoglycaemia (CBG was normal in the stem)
- Thiamine = for Wernicke's encephalopathy (alcohol-related)
9. Integration with Related Lectures
- Alcohol dependence is covered in detail in GC 161; the CAGE questionnaire from GC 166 directly applies
- Delirium tremens = medical emergency from alcohol withdrawal (seizures, autonomic instability, confusion, visual hallucinations)
- Management: benzodiazepines (chlordiazepoxide/diazepam tapering regimen), thiamine, supportive care
- 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
- BZDs and sleeping pills are not for long-term management of any psychiatric condition [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: which drugs are addictive? BZDs for long-term management? (Answer: NO) [1]
- Substance-induced psychosis vs. schizophrenia — visual hallucinations = key 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 is only ONE component; addiction also requires social/personal decline, tolerance, and psychological dependence |
| "All drugs work through dopamine" | All activate mesolimbic DA system, but some also have dopamine-independent reinforcement at NAcc (cannabinoids via CB1, opiates via 5-HT) |
| "Tolerance = needing more drug" only | Tolerance is due to neuroplasticity — receptor downregulation and post-receptor adaptation; it has a mechanistic basis |
| "Personality doesn't matter" | Lecture says it's controversial but still relevant: sensation-seeking → experimentation; obsessional/anxious → dependence |
| "Relapse = treatment failure" | Relapse is a normal part of the stages-of-change cycle; it's "fall from the grace," not the end |
Past Paper Questions
Stem: "A 23-year-old university student presented to the A&E with auditory hallucinations, visual hallucinations, persecutory delusion, passivity experience and disorganised speech. He had a recent history of amphetamine abuse. Which of the following clinical features indicates substance-induced psychosis, rather than schizophrenia, is the MOST LIKELY diagnosis?" [5]
Options: A. Disorganised speech B. Passivity experience C. Persecutory delusion D. Visual hallucinations
Answer: D. Visual hallucinations
Rationale: Visual hallucinations are much more characteristic of organic/substance-induced psychosis than primary schizophrenia (which predominantly features auditory hallucinations). Passivity experience is a first-rank symptom of schizophrenia. Persecutory delusions and disorganised speech can occur in both.
Stem: "You have just received a confused middle-aged male patient in the A&E. ... malnourished and snoring adult. BP 95/65, HR 50, RR 8, SpO2 90%, GCS E2V1M5. Pupils are pinpoint. Contracted scars in groin areas. CBG 4 mmol/L. Which drug would have the BEST chance of improving the mental status?" [6]
Options: A. Dextrose B. Flumazenil C. Naloxone D. Thiamine
Answer: C. Naloxone
Rationale: Pinpoint pupils + respiratory depression + decreased consciousness + groin scars (IV drug use) = classic opioid overdose. Naloxone is a competitive opioid receptor antagonist. CBG is normal (4 mmol/L) so dextrose is unnecessary. Flumazenil is for benzodiazepine overdose (pupils would not be pinpoint). Thiamine is for Wernicke's (not this presentation).
This EMQ set on "Common Psychological Presentations" lists "Substance use disorder" as option I [8]. While the specific stems for Q23–27 don't directly test substance use disorder (Q23 = GAD, Q24 = Depression, Q25 = Panic disorder, Q26 = MDD, Q27 = OCD), the examiner explicitly includes substance use disorder in the differential list, showing it is expected knowledge for psychiatric EMQs.
Stem: "It has been advocated by some people that moderate consumption of alcoholic beverages can help to reduce risk of coronary heart disease. (a) What is the meaning of moderate alcohol consumption? (b) How much pure alcohol does a standard drink contain? (c) What amount of liquor, wine, and beer is a standard drink? (d) What is the recommendation by the American Heart Association regarding alcohol use for cardioprotection for non-drinker and established moderate drinkers?" [9]
This tests alcohol-specific knowledge — primarily GC 161 territory but relevant to the assessment component of GC 166 (quantifying use). Key answers: moderate = ≤2 standard drinks/day for men, ≤1/day for women; 1 standard drink = ~10g pure alcohol (WHO) or ~14g (US); AHA does NOT recommend starting alcohol for cardioprotection in non-drinkers.
High Yield Summary
-
Terminology hierarchy: Problem use → Craving → Dependence (physical + psychological) → Addiction (extreme end with social decline). 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, dopamine, positive reinforcement) → Tolerance/Withdrawal (receptor downregulation, extended amygdala, CRF/NE, negative reinforcement) → Craving/Preoccupation (amygdala + hippocampus + PFC, glutamate, conditioned cues/stress). Failed top-down control by frontal cortex perpetuates the cycle.
-
D2 receptors are persistently decreased in addicts (Volkow 1999) — explains both tolerance and vulnerability.
-
All drugs of abuse activate the mesolimbic DA system but some also have DA-independent reinforcement at NAcc (cannabinoids via CB1, opiates via 5-HT).
-
CAGE questionnaire: Cut down, Annoyed, Guilty, Eye-opener. ≥2 positive = further assessment warranted.
-
Why people use drugs matters for treatment: only ~20% purely for pleasure; reasons are dynamic; self-medication of psychiatric comorbidity is extremely common.
-
Route matters: IV > inhalation > oral in terms of reinforcing potential and risk.
-
Prochaska & DiClemente Stages of Change: Pre-contemplation → Contemplation → Preparation → Action → Maintenance → Relapse (cyclical, not linear).
-
Substance-induced psychosis: visual hallucinations are the key discriminator from schizophrenia.
-
Opioid overdose triad: pinpoint pupils + respiratory depression + decreased consciousness → naloxone.
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)
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