Substance Use Disorder

Department of Health and Social Care Guidance Drug misuse and dependence: UK guidelines on clinical management. Last updated: Aug 2026.

Article Last Updated:25/08/2026

Substance Use Disorder

This article covers:

Substance use disorder as a whole
Commonly misused substances, including:
- Cocaine
- Cannabis
- MDMA (ecstasy)
- LSD
- Ketamine

Substance Use Disorder Overview

Risk Factors

^[Ref]

Family history of substance use disorder
Concurrent mental health conditions, esp.
- Depression and other mood disorders
- Anxiety disorders
- ADHD
- Psychotic disorders
- Personality disorders
Childhood adversity and trauma
Environmental and social factors (e.g. exposure to substance use within the family or peer group, socioeconomic disadvantage and stressful living environments)
Early initiation of substance use
Greater availability and exposure to substances

Diagnostic Criteria

High-yield pattern recognition for substance use disorder:

Substance use disorder should be considered when substance use becomes persistent and problematic, causing:

Loss of control → using more than intended, unsuccessful attempts to cut down, craving, or spending substantial time obtaining/using/recovering from the substance
Impaired functioning → problems at work, education, home or in relationships; reducing or giving up important activities
Continued use despite harm → recurrent or continued use despite recognised physical or psychological consequences
Physiological adaptation → tolerance and/or withdrawal

NB Diagnosis does not require all 4 patterns, see below for more details.

DSM-5 criteria for substance use disorder require≥2 of the 11 criteria occurring within the same 12-month period: ^[Ref]

Criteria	Description
Impaired control over substance use	Consuming the substance in larger amounts and for a longer amount of time than intended Persistent desire to cut down or regulate use. The individual may have unsuccessfully tried to stop in the past Spending a great deal of time obtaining, using, or recovering from the effects of substance use Experiencing craving, a pressing desire to use the substance
Social impairment	Substance use impairs ability to fulfil major obligations at work, school, or home Continued use of the substance despite it causing significant social or interpersonal problems Reduction or discontinuation of recreational, social, or occupational activities because of substance use
Risky use	Recurrent substance use in physically unsafe environments Persistent substance use despite knowledge that it may cause or exacerbate physical or psychological problems
Pharmacologic	Tolerance: Individual requires increasingly higher doses of the substance to achieve the desired effect, or the usual dose has a reduced effect; individuals may build tolerance to specific symptoms at different rates Withdrawal: A collection of signs and symptoms that occurs when blood and tissue levels of the substance decrease, individuals are likely to seek the substance to relieve symptoms NB there is no characteristic withdrawal syndrome for hallucinogens, phencyclidine and inhalants, therefore the withdrawal criterion generally cannot be met for those substances NB Tolerance and withdrawal in the context of appropriate medical treatment (i.e. pain medication used as prescribed) do NOT count as criteria

Severity is then based on the total number of the criteria met:

Mild: 2–3 criteria
Moderate: 4–5 criteria
Severe: ≥6 criteria

UK Controlled Drug Classification

Under the Misuse of Drugs Act 1971, controlled drugs are classified as Class A, B or C according to their assessed potential harm to the individual and society

Class A → generally considered the most harmful and carries the highest legal penalties
Class B → intermediate classification
Class C → generally considered lower harm than Class A or B and carries lower penalties

NB This is a legal classification and should not be used alone to determine the clinical toxicity or severity of intoxication in patients ^[Ref]

Class	Common examples
A	Cocaine MDMA (ecstasy) Methamphetamine (crystal meth) Heroin Fentanyl LSD Magic mushrooms
B	Cannabis Amphetamine Keatmine Codeine Methylphenidate GHB / GBL Barbiturates
C	Benzodiazepines Pregabalin / gabapentin Buprenorphine Anabolic steroids Nitrous oxide

High-Yield Substances

Alcohol

Alcohol use disorder (including alcohol withdrawal, alcohol misuse) is covered separately in a dedicated article as it is clinically important and has distinct intoxication, withdrawal and management pathways.

See the Alcohol Use Disorders article.

Opioids

Opioid misuse (including opioid intoxication, opioid withdrawal) is covered separately in a dedicated article as it is clinically important and has distinct intoxication, withdrawal and management pathways.

See the article.

Opioids are a drug class, not one specific drug

However, “opioid” is a pharmacological class, not a Class A/B/C category
For instance, heroin, fentanyl and methadone are Class A, while codeine is Class B

Common examples include:

Morphine
Codeine
Fentanyl
Oxycodone
Heroin (diamorphine)

Opiates vs opioids

Opiates = naturally derived from opium, e.g. morphine and codeine
Opioids = broader term covering natural, semi-synthetic and synthetic opioid drugs, e.g. heroin, fentanyl, methadone

Cocaine

Domain

Subcategory

Key information

Overview ^[Ref]

Common names / examples

There are 2 main forms of cocaine:

Powder cocaine (cocaine hydrochloride) → usually snorted (less commonly injected)
Crack cocaine (free-based cocaine) → usually smoked

Drug class / MoA

Drug class: CNS / sympathomimetic stimulant

MoA:

Primarily inhibits presynaptic monoamine reuptake (esp. dopamine)
- ↑ Dopamine → euphoria and reinforcing / addictive effects
- ↑ Noradrenaline → sympathetic effects
Also inhibits voltage-gated sodium channels (→ local anaesthetic effects)

Acute effects ^[Ref]

Intoxication / expected acute effects

CNS stimulant / dopaminergic effects:

Euphoria
Increased alertness
Increased energy
Reduced appetite
Feeling powerful / confident
May progress to agitation / hyperstimulation

Sympathomimetic effects:

Tachycardia
Hypertension
Mydriasis
Diaphoresis
Hyperthermia

Acute toxicity / overdose features

Neuropsychiatric:

Severe anxiety
Agitation / aggression
Seizures
Delirium / acute psychosis (e.g. hallucinations, delusions)

Cardiovascular:

Coronary vasospasm → myocardial ischaemia +/- infarction
Severe hypertension
Stroke
Aortic dissection
Arrhythmias

Systemic and other:

Hyperthermia
Rhabdomyolysis
Intestinal ischaemia
Severe toxicity may lead to renal failure and coagulopathy

Cocaine toxicity is usually a clinical diagnosis

Urine toxicology screen serves as a confirmatory test
Serum cocaine levels are typically NOT measured and not required for diagnosis
Additional investigations for cocaine-related chest pain
- Suspected myocardial ischaemia: serial ECG, troponin, chest X-ray)
- Suspected aortic dissection: ECG, chest X-ray, CT chest)

General initial toxicology work-up:

Metabolic panel (U&Es, bone profile)
Blood gas, including lactate level
Serum paracetamol, salicylate and ethanol concentrations
Urinalysis and urine toxicology screen

Acute management

There is no antidote for cocaine, management is targeted at symptoms

Mild intoxication usually requires NO treatment due to the short half-life of cocaine

Management for more severe intoxication:

Severe agitation / hypertension / seizures → benzodiazepines
- Consider IV nitrates / nicardipine if hypertension persists despite benzodiazepines
Hyperthermia → IV fluids, active cooling, sedation
Suspected myocardial ischaemia should be managed as acute coronary syndrome

Avoid beta blockers in acute cocaine toxicity

Long-term effects ^[Ref]

Complications from chronic use

Repeated intranasal use → nasal septal perforation
Cardiomyopathy
Cognitive impairment
Interstitial pneumonitis / pulmonary fibrosis (from frequent inhalation of contaminated cocaine)

Withdrawal features

Withdrawal symptoms develop quickly as cocaine has a short half-life:

Post-cocaine “crash”
Somnolence
Difficulty concentrating
Increased appetite

Long-term management

There is no medication to treat cocaine dependence or withdrawal symptoms

Mainstay is psychosocial interventions:

Contingency management (incentives for abstinence) – strongest evidence
CBT
Community reinforcement approach
Family, couples and social network interventions
Peer groups

Manage any comorbid conditions (e.g. depression)

Cannabis

Domain

Subcategory

Key information

Overview ^[Ref]

Common names / examples

Cannabis is a psychoactive drug derived from the Cannabis plant

Weed (marijuana) is a specific type of cannabis preparation, which is dried cannabis plant material

Drug class / MoA

Cannabis contains multiple cannabinoids, which are chemicals that act on the cannabinoid system

THC is the main psychoactive / intoxicating cannabinoid (i.e. the main intoxicating component)
THC acts as a partial agonist at cannabinoid CB1 and CB2 receptors
- CB1 receptors are mainly expressed in the CNS
- Activation of CB1 receptors alters neurotransmitter release → affects mood, perception, memory, coordination and appetite

Acute effects ^[Ref]

Intoxication / expected acute effects

Psychological / CNS effects

Euphoria and relaxation
- The characteristic “high” with cannabis use is relaxation / dreamy / altered perception
- Rather than marked stimulation seen with stimulant drugs
Altered time, colour and spatial perception
Impaired concentration, reaction time, fine coordination
Increased appetite
Anxiety, panic or paranoia may occur (esp. in inexperienced users)

Physical effects

Tachycardia
Conjunctival injection
Dry mouth

Acute toxicity / overdose features

Acute cannabis toxicity is usually mild and self-limiting

Mainly causes neuropsychiatric effects

Marked anxiety
Paranoia
dysphoria
Psychotic symptoms may be precipitated or exacerbated (esp. in susceptible individuals)

High doses in young children may cause respiratory depression

Acute management

Most patients require observation and supportive care only

Management of hyperemesis syndrome

IV fluids + antiemetics
Definitive management = cessation of cannabis use

Long-term effects ^[Ref]

Complications from chronic use

Cannabinoid hyperemesis syndrome (recurrent / cyclical episodes of nausea and vomiting)
Respiratory
- Chronic cough
- Wheeze
- Increased sputum
- Recurrent acute bronchitis
Cognitive impairment +/- hippocampal structural changes
Reduced fertility
Chronic heavy use is associated with risk of
- Psychotic disorders (e.g. schizophrenia)
- Depression, anxiety
- Other substance use disorder

Withdrawal features

Cannabis withdrawal is usually mild and may occur after stopping frequent, heavy use:

Insomnia
Irritability
Depression
Nausea
Reduced appetite

Long-term management

There is no medication to treat cannabis dependence or withdrawal symptoms

Mainstay is psychosocial interventions:

Less dependent users → brief motivational interventions
Heavily dependent users → structured care-planned intervention
- Motivational enhancement
- CBT
- Contingency management (incentives for abstinence)

Manage any comorbid conditions (e.g. depression)

MDMA (Ecstasy)

MDMA vs ecstasy vs methamphetamine vs crystal meth

Domain

Subcategory

Key information

Overview ^[Ref]

Common names / examples

MDMA = 3, 4-methylenedioxymethamphetamine

Common recreational names:

Ecstasy (often marketed as tablets)
Molly (often marketed as powder / crystals)

Drug class / MoA

Class: substituted amphetamine with stimulant and empathogenic effects

MoA: increases pre-synaptic monoamine neurotransmitter concentrations

Serotonin (prominent effect) → mood elevation, altered perception, empathogenic effects
Dopamine → stimulant / reward effects
Noradrenaline → sympathetic effects

Do not confuse related amphetamine-type drugs:

Amphetamine = a stimulant drug (e.g. dexamfetamine used for ADHD)
Methamphetamine (meth / crystal meth) = a related stimulant with predominantly dopaminergic and noradrenergic effects
MDMA (ecstasy / molly) = a related substituted amphetamine with more prominent serotonergic effects

Acute effects ^[Ref]

Intoxication / expected acute effects

Neuropsychiatric effects

- Excitement and disinhibition
- Increased empathy and feelings of interpersonal closeness
- Heightened physical sensation
- Euphoria
- Difficulty concentrating
- May cause a sense of ego dissolution

(feeling “at one” with the world)

Sympathetic effects

Tachycardia
Hypertension
Mydriasis
Hyperthermia

Acute toxicity / overdose features

SIADH → hyponatraemia
- Severe hyponatraemia may cause cerebral oedema → altered mental status and seizures
Sympathomimetic toxicity
- Tachycardia, tachyarrhythmias, hypertension
- Hyperthermia
- Agitation, hyperactivity, seizures
Hyperthermia-related complications
- Rhabdomyolysis
- Multiorgan failure
- Coagulopathy

MDMA toxicity is typically a clinical diagnosis

Important investigations:

ECG + cardiac monitoring
Serum sodium level (if hyponatraemia is present → paired serum + urine osmolality + urine sodium)
Renal function

Serum MDMA concentration is rarely required

General initial toxicology work-up:

Metabolic panel (U&Es, bone profile)
Blood gas, including lactate level
Serum paracetamol, salicylate and ethanol concentrations
Urinalysis and urine toxicology screen

Acute management

Benzodiazepines (IM / IV) for agitation, tachycardia, hypertension, seizures
External cooling for hyperthermia
Isotonic IV fluids for hyponatraemia (severe hyponatraemia may require hypertonic saline) and rhabdomyolysis

Long-term effects ^[Ref]

Complications from chronic use

Dependence
Cognitive decline
Paranoid psychosis

Long-term management

There is no medication to treat MDMA dependence or withdrawal symptoms

Mainstay is psychosocial interventions

LSD (Lysergic Acid Diethylamide)

LSD is a classic hallucinogen

Domain

Subcategory

Key information

Overview ^[Ref]

Common names / examples

LSD = lysergic acid diethylamide

Common recreational name: acid

Drug class / MoA

Class: semi-synthetic classic hallucinogen (psychedelic)

Primary MoA: 5-HT (serotonin) receptor agonist

Acute effects ^[Ref]

Intoxication / expected acute effects

Neuropsychiatric effects

Altered perception with intensification of sensations (e.g. intensified colours, distorted vision)
Synesthesia (e.g. “seeing sounds” or “hearing colours”)
Altered sense of reality
Depersonalisation (feeling that the self is unreal)
Mood changes (usually euphoria, but may be depressive)
Impaired judgement

Despite LSD being classed as a hallucinogen, true hallucinations and delusions are uncommon, perceptual distortion is more typical.

Physical effects

Mydriasis
Blurred vision
Sweating
Palpitations
Impaired coordination

Acute toxicity / overdose features

Severe LSD toxicity is uncommon

Neuropsychiatric

Severe anxiety
Extreme apprehension or agitation
Delusions or true hallucinations

Systemic

Hyperthermia
Tachyarrhythmia
Cardiovascular instability in massive overdose

Acute management

Most cases: observation in a quiet, calming environment + reassurance

Consider benzodiazepines for severe anxiety / agitation

External cooling + benzodiazepines for hyperthermia

Long-term effects ^[Ref]

Complications from chronic use

Hallucinogen persistent perception disorder (HPPD) / “flashbacks”

Recurrent perceptual disturbances after the drug has been stopped
Usually involves visual illusions, but can also involve distortions of
- Other senses
- Self-image
- Time
- Space

Withdrawal features

No characteristic withdrawal syndrome is recognised

Physical dependence is not a typical feature of LSD use

Long-term management

Mainstay is psychosocial interventions

No medications

Ketamine

Domain

Subcategory

Key information

Overview ^[Ref]

Common names / examples

Common recreational names include ket and K

Drug class / MoA

Class: dissociative anaesthetic agent

MoA: NMDA glutamate receptor non-competitive antagonist

Acute effects ^[Ref]

Intoxication / expected acute effects

Neuropsychiatric effects

Inappropriately elevated mood
Dissociation (feeling detached from oneself or the environment)
Depersonalisation
Altered responses to external stimuli

Physical effects

Nystagmus
Tachycardia

Acute toxicity / overdose features

Marked dissociation + depersonalisation
Seizures
Coma
Tachycardia, severe hypertension, arrhythmias
Hyperthermia
Acidosis
Laryngospasm

Acute management

Most cases: supportive care (keep in a quiet, calming environment) + close observation

Benzodiazepines for agitation or seizures

Long-term effects ^[Ref]

Complications from chronic use

Ketamine cystitis (“ketamine bladder”)
- Dysuria
- Urinary frequency
- Haematuria
Biliary colic
Memory impairment

Withdrawal features

No characteristic withdrawal syndrome is recognised

Long-term management

Mainstay is psychosocial interventions

No medications

References

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Substance Use Disorder

Substance Use Disorder

Substance Use Disorder Overview

Risk Factors

Diagnostic Criteria

UK Controlled Drug Classification

High-Yield Substances

Alcohol

Opioids

Cocaine

Cannabis

MDMA (Ecstasy)

LSD (Lysergic Acid Diethylamide)

Ketamine

References

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