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Adverse drug reactions

SNOMED: 396079007865 words•Updated 03/03/2026
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Exam Tips

  • In OSCEs, classify ADRs quickly as Type A (predictable, dose-related) versus Type B (unpredictable, often immune).
  • Always link symptoms to a medication timeline: start date, dose change, dechallenge response, and interaction history.
  • State high-risk groups explicitly: older adults, renal/hepatic impairment, pregnancy, and polypharmacy.
  • For severe reactions, say: stop culprit drug, treat ABC first, document allergy, and report via MHRA Yellow Card.
  • Use concrete examples: warfarin-bleeding and opioid-respiratory depression (Type A), penicillin anaphylaxis (Type B).
  • Mention that many ADRs are preventable with medication reconciliation, monitoring plans, and patient counselling.

Definition

An adverse drug reaction (ADR) is a harmful, unintended response to a medicine given at normal therapeutic use, and it can also occur with off-label use, medication error, misuse, overdose, or occupational exposure. In clinical practice, ADRs are distinguished from expected therapeutic effects and are a major cause of avoidable morbidity, emergency admission, and treatment discontinuation.

Pathophysiology

ADR mechanisms are classically divided into Type A (dose-related, predictable from pharmacology) and Type B (non-dose-related, unpredictable, often immune-mediated or idiosyncratic). Type A reactions are common (around 80% of ADRs) and reflect exaggerated pharmacodynamic effects (for example, bleeding with warfarin or respiratory depression with opioids), while Type B includes reactions such as penicillin anaphylaxis and severe cutaneous eruptions. Extended classification includes Type C (chronic/continuing toxicity), Type D (delayed toxicity), and Type E (withdrawal effects). Mechanistically, ADRs may arise from altered pharmacokinetics (renal/hepatic impairment, drug interactions), receptor sensitivity changes, pharmacogenomic susceptibility (for example HLA-associated immune risk), or immune hypersensitivity pathways (including IgE-mediated immediate reactions and T-cell-mediated delayed reactions). See Figure reference: Type A-E ADR classification diagram and timeline of onset in standard clinical pharmacology teaching figures.

Risk Factors

  • Polypharmacy and drug-drug interactions
  • Older age and frailty
  • Renal impairment or hepatic dysfunction
  • Previous ADR history, especially prior drug allergy
  • High-risk medicines (anticoagulants, antiplatelets, insulin/sulfonylureas, diuretics, cytotoxics, immunosuppressants, antibiotics)
  • Multiple comorbidities and frequent transitions of care
  • Pregnancy and breastfeeding (altered pharmacokinetics and fetal/neonatal risk)
  • Ethnicity/genetic susceptibility affecting metabolism or immune response
  • Alcohol use, smoking, OTC/herbal/supplement co-use

Clinical Features

Symptoms

  • New rash, pruritus, urticaria, mucosal soreness
  • Dyspnoea, wheeze, throat tightness, dizziness after drug exposure
  • Nausea, vomiting, abdominal pain, diarrhoea
  • Confusion, drowsiness, agitation, insomnia (including withdrawal states)
  • Easy bruising, epistaxis, melaena or haematuria
  • Jaundice, dark urine, reduced urine output, myalgia

Signs

  • Hypotension, tachycardia, hypoxia in severe acute reactions
  • Angioedema, widespread urticaria, bronchospasm
  • Fever with rash or eosinophilia suggestive of severe hypersensitivity
  • Petechiae, ecchymoses, active bleeding
  • Abnormal capillary glucose (hypoglycaemia/hyperglycaemia) in antidiabetic ADRs
  • Organ-specific abnormalities (for example, raised JVP/oedema with fluid-retaining drugs)

Investigations

Structured drug history and temporal correlation:Onset of symptoms after starting/increasing a medicine, with improvement on withdrawal (dechallenge) and recurrence on re-exposure (if it occurred unintentionally)
Medication reconciliation including OTC/herbal agents:Potential interaction, duplication, recent dose error, or contraindicated co-prescription
FBC, U&E, LFT, CRP, clotting profile:Evidence of marrow suppression, renal/hepatic injury, inflammation, or coagulopathy attributable to drug exposure
Drug-specific monitoring (for example INR, drug levels where applicable):Supratherapeutic markers consistent with Type A toxicity (for example elevated INR in warfarin-associated bleeding)
Urinalysis and ECG where indicated:End-organ effects (for example nephrotoxicity) or QT prolongation/arrhythmia risk from culprit medicine
Allergy/immunology referral tests when appropriate:Supportive evidence for true immune-mediated reaction and guidance on future avoidance
Yellow Card reporting documentation:Suspected ADR recorded and submitted, especially for serious, unusual, or black triangle medicine reactions

Management

Lifestyle Modifications

  • Give clear counselling on suspected culprit drugs and class cross-reactivity risk
  • Advise patients to carry an up-to-date medicines/allergy list and present it at every healthcare contact
  • Reduce avoidable interaction risks (alcohol excess, unreviewed OTC/herbal products)
  • Arrange regular medication review, especially in older adults with polypharmacy
  • Use safety-net advice: urgent help for breathlessness, facial swelling, syncope, extensive rash, mucosal involvement, or bleeding

Pharmacological Treatment

Immediate withdrawal and supportive care

  • Stop suspected offending medicine(s) promptly
  • Switch to safer alternative within same therapeutic goal where possible

Avoid re-challenge after severe reactions (for example anaphylaxis, SJS/TEN, DRESS, AGEP, drug-induced liver failure). Document allergy/ADR clearly in prescribing systems.

Anaphylaxis treatment (adult)

  • Adrenaline (epinephrine) 500 micrograms IM (0.5 mL of 1 mg/mL [1:1000]), repeat every 5 minutes if needed
  • Chlorphenamine 10 mg IV/IM after initial resuscitation
  • Hydrocortisone 200 mg IV after initial resuscitation

Adrenaline is first-line; do not delay for antihistamines or steroids. Give high-flow oxygen and IV fluids as required. Observe for biphasic reaction.

Selected antidote-based management for severe drug toxicity presentations

  • Naloxone 400 micrograms IV, repeated every 2-3 minutes to adequate ventilation (up to 10 mg total if required) for opioid toxicity
  • Acetylcysteine IV for significant paracetamol toxicity: 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours
  • Warfarin major bleeding: 4-factor prothrombin complex concentrate plus phytomenadione 5 mg IV

Use local toxicology/BNF protocols and senior input. Titrate naloxone to respiratory effort to avoid abrupt withdrawal. Reverse anticoagulation urgently in life-threatening bleeding.

Monitoring and prevention of recurrence

  • Dose reduction or interval extension based on renal/hepatic function
  • Prophylactic gastroprotection when indicated (for example proton pump inhibitor with high GI bleed risk NSAID/antiplatelet regimens)

Check contraindications before re-prescribing (for example previous true penicillin anaphylaxis contraindicates re-exposure to culprit penicillin). Intensify biochemical monitoring for high-risk drugs.

Complications

  • Emergency hospital admission and prolonged inpatient stay
  • Preventable morbidity from bleeding, hypoglycaemia, falls, arrhythmia, renal/hepatic injury
  • Severe hypersensitivity syndromes (anaphylaxis, SJS/TEN, DRESS) with risk of organ failure
  • Death in severe ADR presentations
  • Reduced adherence and loss of confidence in medicines/health services
  • Diagnostic delay when ADR mimics new disease

Prognosis

Most ADRs improve with early recognition, prompt withdrawal of the culprit medicine, and targeted supportive treatment. Prognosis worsens with delayed diagnosis, polypharmacy, frailty, and severe immune-mediated or organ-toxic reactions; however, many serious outcomes are preventable through safer prescribing, monitoring, and pharmacovigilance reporting.

Sources & References

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 308)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 146, 147)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 320, 321)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1686)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1751, 1752)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1631)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1685, 1686)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1604, 1605)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1838, 1839)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 311)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 147)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1605)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 311, 312)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 148)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1843)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 870)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1805)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1658)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1761)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 342, 343)[context]

Sources

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