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ukmla 2026

Alcohol Use Disorder

Harmful or dependent pattern of alcohol use causing physical, psychological, or social harm — managed with psychosocial interventions, medically assisted withdrawal, and relapse prevention pharmacotherapy

Psychiatrycommonchronic
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Condition details
Psychiatry
common
7 min read
reviewed 2026-04-05
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About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

  • AUDIT questionnaire for screening: 8–15 hazardous, 16–19 harmful, ≥20 probable dependence
  • Dependence features: tolerance, withdrawal, compulsive use, continued use despite harm, neglecting obligations
  • Medically assisted withdrawal: chlordiazepoxide reducing regimen over 5–10 days + thiamine (IV Pabrinex then oral)
  • Alcohol withdrawal: tremor (6–12h) → seizures (24–48h) → delirium tremens (48–72h) — DTs are life-threatening
  • Relapse prevention: acamprosate (first-line) or naltrexone + psychosocial intervention (motivational interviewing, CBT)
  • Wernicke encephalopathy: confusion + ataxia + ophthalmoplegia → treat with IV Pabrinex BEFORE glucose to prevent Korsakoff syndrome

Overview

Alcohol use disorder encompasses a spectrum from hazardous drinking (increased risk of harm) through harmful use (alcohol causing physical or psychological damage) to alcohol dependence (compulsive use despite harm, tolerance, and withdrawal). Alcohol dependence is characterised by a strong desire to drink, difficulty controlling use, withdrawal symptoms on cessation, tolerance (needing more for the same effect), neglecting alternative pleasures, and continued use despite harm. Alcohol is a CNS depressant that acts primarily through GABA potentiation and NMDA receptor inhibition. Chronic use causes neuroadaptation; abrupt cessation leads to CNS excitation (withdrawal). Alcohol misuse is a major public health issue, contributing to liver disease, pancreatitis, cardiovascular disease, cancer, depression, and social harm.

Epidemiology

Approximately 24% of adults in England drink above the recommended 14 units per week. Harmful drinking and dependence affect approximately 4–5% and 1.5% of adults respectively. Alcohol-related hospital admissions exceed 1 million per year in England. Alcohol is responsible for approximately 10,000 deaths annually in the UK. It is more common in men (3:1 ratio) and peaks in middle age. Risk factors include male sex, family history, early onset drinking, mental health disorders (depression, anxiety, PTSD), social deprivation, occupational exposure (hospitality, military), and adverse childhood experiences.

Clinical Features

Symptoms
Craving: strong urge or compulsion to drink alcohol
Loss of control: difficulty limiting the amount consumed once started
Tolerance: needing increasing amounts for the same effect
Withdrawal symptoms: tremor, sweating, anxiety, nausea, insomnia, seizures on cessation
Continued drinking despite physical, psychological, or social harm
Neglecting responsibilities: work, family, social obligations
Morning drinking, secretive drinking, narrow drinking repertoire
Delirium tremens: confusion, visual hallucinations, severe tremor, tachycardia, fever (48–72h after last drink)
Signs
Tremor (fine resting tremor, worse on intention)
Alcohol on breath, signs of self-neglect
Spider naevi, palmar erythema, gynaecomastia (chronic liver disease)
Hepatomegaly, jaundice, ascites (advanced liver disease)
Wernicke encephalopathy triad: confusion + ataxia + ophthalmoplegia (nystagmus, lateral rectus palsy)

Investigations

First-line
AUDIT questionnaireAlcohol Use Disorders Identification Test: 10 questions. 8–15 hazardous, 16–19 harmful, ≥20 probable dependence. AUDIT-C (3 questions) for brief screening
SADQSeverity of Alcohol Dependence Questionnaire: 20 items. Mild <16, moderate 16–30, severe >30 — guides setting for detox (community vs inpatient)
BloodsFBC (macrocytosis/raised MCV), LFTs (raised GGT most sensitive, raised AST:ALT ratio >2:1 suggests alcoholic liver disease), U&Es, clotting, glucose, magnesium
Second-line
CDT (carbohydrate-deficient transferrin)Most specific biomarker for chronic heavy alcohol use — can also monitor abstinence
Liver ultrasoundAssess for steatosis, fibrosis, cirrhosis
FibroScanNon-invasive assessment of liver fibrosis/cirrhosis
Specialist
Psychiatric assessmentAssess for comorbid depression, anxiety, PTSD, personality disorder — very common in alcohol dependence
1
Brief intervention (hazardous/harmful drinkers)
  • Brief advice (5–10 min) on reducing alcohol intake — effective at reducing consumption
  • Extended brief intervention: motivational interviewing (20–30 min) for harmful drinkers
  • Advise on UK CMO guidelines: ≤14 units/week, spread over 3+ days, with alcohol-free days
2
Medically assisted withdrawal (dependent drinkers)
  • Chlordiazepoxide reducing regimen: typical starting dose 20–30 mg QDS, reducing over 5–10 days
  • Community detox if: mild-moderate dependence (SADQ <30), stable housing, supportive environment, no history of withdrawal seizures/DTs
  • Inpatient detox if: severe dependence (SADQ >30), history of seizures or DTs, significant comorbidity, no social support, previous failed community detox
  • Thiamine replacement: IV Pabrinex for ≥3 days (if any risk of Wernicke), then oral thiamine 100 mg TDS long-term
3
Relapse prevention
  • Acamprosate: first-line (start after detox, continue 6–12 months). Modulates glutamate/GABA to reduce craving
  • Naltrexone: alternative (opioid antagonist — reduces rewarding effects of alcohol)
  • Disulfiram: deterrent therapy (causes unpleasant flushing, nausea, headache if alcohol consumed) — requires supervised administration
  • Psychosocial interventions: CBT, behavioural couples therapy, social network therapy, 12-step facilitation
4
Wernicke encephalopathy prevention
  • IV Pabrinex (thiamine) to ALL patients with suspected or at-risk Wernicke encephalopathy
  • Give thiamine BEFORE glucose — glucose without thiamine can precipitate Wernicke in thiamine-depleted patients
  • Wernicke triad (confusion, ataxia, ophthalmoplegia) is present in only ~10% — have a low threshold for treatment
  • Untreated Wernicke → Korsakoff syndrome: irreversible anterograde amnesia, confabulation

Complications

  • Alcohol withdrawal seizures: Typically 24–48h after last drink — generalised tonic-clonic
  • Delirium tremens: 48–72h — confusion, visual hallucinations, tremor, fever, autonomic instability. 5–15% mortality untreated
  • Wernicke-Korsakoff syndrome: Thiamine deficiency → Wernicke (reversible) → Korsakoff (irreversible amnesia + confabulation)
  • Alcoholic liver disease: Steatosis → hepatitis → cirrhosis → hepatocellular carcinoma
  • Pancreatitis: Acute and chronic — alcohol is the second most common cause in the UK
  • Cancers: Liver, oesophageal, oropharyngeal, breast, colorectal
UKMLA Exam Tips
  • 1Alcohol withdrawal timeline: tremor 6–12h → seizures 24–48h → delirium tremens 48–72h
  • 2Chlordiazepoxide is the standard benzodiazepine for alcohol withdrawal — reducing regimen over 5–10 days
  • 3Give thiamine (Pabrinex) BEFORE glucose — glucose can precipitate Wernicke in thiamine-depleted patients
  • 4Wernicke triad (confusion + ataxia + ophthalmoplegia) is complete in only ~10% — treat on suspicion alone
  • 5AST:ALT ratio >2:1 is characteristic of alcoholic liver disease (in most liver diseases, ALT > AST)
  • 6Acamprosate is first-line for relapse prevention. Naltrexone is the alternative. Disulfiram is deterrent-based
  • 7AUDIT ≥20 suggests probable dependence. SADQ >30 = severe dependence requiring inpatient detox
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Verified Sources & References

NICE CG115 — Alcohol-use disorders: diagnosis, assessment and management
NICE CG100 — Alcohol-use disorders: management of physical complications