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MRCP PART 1 · CLINICAL PHARMACOLOGY AND THERAPEUTICS

Clinical pharmacology and therapeutics questions
for MRCP Part 1.

Clinora has 346 clinical pharmacology and therapeutics single best answer questions covering 326 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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Question 1Adverse drug reactionsMedium

A patient develops a severe, unexpected mucocutaneous reaction shortly after starting a new anticonvulsant. Which action is most appropriate regarding regulatory reporting in the UK?

  1. AOnly pharmaceutical companies are permitted to report suspected reactions
  2. BNo reporting is needed if the reaction is already listed in the product literature
  3. CReport the suspected adverse drug reaction via the Yellow Card Scheme
  4. DReporting is only required for reactions leading to death
  5. EWait for definitive causality proof before reporting
Show answer and explanation

Answer: C Report the suspected adverse drug reaction via the Yellow Card Scheme

A severe mucocutaneous reaction soon after starting an anticonvulsant (for example carbamazepine, lamotrigine or phenytoin) raises the possibility of Stevens–Johnson syndrome or toxic epidermal necrolysis. Clinically, stop the suspected drug and get urgent specialist care. For regulation, report it to the MHRA through the Yellow Card scheme. Suspicion is enough: proof of causality is not needed. Healthcare professionals, patients and carers can all report. Serious reactions should be reported even if they are already listed in the product information, because the reports feed signal detection and estimates of frequency. For black triangle (▼) medicines, which are under additional monitoring, report all suspected reactions, however minor.

Key clue
Suspected serious drug reaction requiring regulatory reporting
What it means
Reportable suspected adverse drug reaction
What to do
Submit a Yellow Card report promptly and manage the reaction clinically, stopping the likely causative drug

Why the other options are less appropriate

  • A Anyone can submit a Yellow Card: healthcare professionals, patients and carers, not only manufacturers.
  • B Serious reactions should be reported even when already listed; reports help the MHRA judge how often and how severely they occur.
  • D Reporting covers all serious suspected reactions, such as those causing hospital admission, disability or that are life-threatening, not only deaths.
  • E A reasonable suspicion is enough to report. Waiting for proof delays signal detection and is not required.

Source: Medicines and Healthcare products Regulatory Agency: Yellow Card Scheme

Question 2Dose-responseMedium

Drug X requires a much lower dose than Drug Y to produce the same magnitude of effect, but both drugs can achieve the same maximum effect. Which pharmacological term best describes the difference between Drug X and Drug Y?

  1. ADrug X has greater efficacy than Drug Y
  2. BDrug X is more potent than Drug Y
  3. CDrug X has a narrower therapeutic index
  4. DDrug X is a partial agonist and Drug Y is a full agonist
  5. EDrug X and Drug Y have identical pharmacodynamic properties
Show answer and explanation

Answer: B Drug X is more potent than Drug Y

The key clue is that both drugs reach the same maximum effect, but Drug X does so at a much lower dose. Potency describes how much drug is needed to produce a given effect and is usually expressed as the EC50, the concentration giving 50% of the maximal response. A more potent drug has a lower EC50, so its dose-response curve sits further to the left. Efficacy (Emax) is the maximum response a drug can produce, shown by the height of the curve's plateau. Here the plateaus are equal, so efficacy is the same. Potency depends on receptor affinity and on how effectively binding is converted into a response. Clinically, efficacy usually matters more than potency, because a less potent drug can simply be given at a higher dose: 1 mg of bumetanide has about the same diuretic effect as 40 mg of furosemide. A partial agonist has lower efficacy than a full agonist however much is given. A competitive antagonist shifts the agonist curve to the right without lowering the maximum, while a non-competitive antagonist lowers the maximum.

Key clue
Different dose needed for same effect, same maximum effect achievable
What it means
Difference in potency, not efficacy
What to do
Recognise Drug X as more potent; potency does not by itself indicate a clinically superior drug

Why the other options are less appropriate

  • A Efficacy is the maximum achievable effect. Both drugs reach the same maximum, so their efficacy is equal.
  • C Therapeutic index compares toxic and effective doses. The stem gives no information about toxicity for either drug.
  • D A partial agonist cannot reach a full agonist's maximum effect, however high the dose. Both drugs here reach the same maximum.
  • E Different doses are needed for the same effect, so their potency differs and their pharmacodynamics are not identical.

Source: StatPearls: Pharmacodynamics

Question 3Withdrawal/deprescribingMedium

A patient who has taken a benzodiazepine daily for two years wishes to stop. What is the most appropriate approach to discontinuation?

  1. AContinue it indefinitely, because withdrawal risks outweigh those of continued use
  2. BStop abruptly, as two years of use is too short to cause dependence
  3. CHalve the dose each week and stop after 2 weeks
  4. DSwitch to zopiclone and stop the benzodiazepine
  5. EA gradual, individualised dose reduction over weeks to months rather than abrupt cessation
Show answer and explanation

Answer: E A gradual, individualised dose reduction over weeks to months rather than abrupt cessation

After two years of daily use, physical dependence is likely, so the question is how to stop safely rather than whether stopping is possible. Long-term benzodiazepine use causes adaptive changes in GABA-A receptor function, so abrupt cessation produces a withdrawal syndrome of anxiety, insomnia, tremor, sweating and perceptual disturbance, and in severe cases seizures and confusion. Withdrawal should be gradual and agreed with the patient. The BNF advises reducing the dose by about one-eighth (range one-tenth to one-quarter) of the daily dose every fortnight, and NICE CKS similarly advises slow tapering with the pace guided by symptoms, so withdrawal may take several months or longer. People taking short-acting drugs such as lorazepam or alprazolam are usually switched to an equivalent dose of diazepam first, because its long half-life smooths fluctuations in blood levels; diazepam 5 mg is roughly equivalent to lorazepam 500 micrograms or temazepam 10 mg. Regular review, psychological support and willingness to slow or pause the taper improve success.

Key clue
Long-term benzodiazepine use with a wish to discontinue
What it means
Benzodiazepine dependence requiring safe tapering
What to do
Develop an individualised gradual tapering plan with regular review and psychological support as needed

Why the other options are less appropriate

  • A Continued use carries risks of falls, cognitive impairment and dependence, and a patient who wishes to stop should be supported to taper.
  • B Dependence can develop after only 4 weeks of regular use. Stopping abruptly after two years risks withdrawal symptoms and seizures.
  • C Halving weekly is far too fast after long-term use. The BNF suggests reducing by about one-eighth of the daily dose every fortnight.
  • D Z-drugs act on the same GABA-A receptors and share the dependence risk, so switching does not withdraw the patient.

Source: NICE CKS: Benzodiazepine and z-drug withdrawal

Question 4Saturation kineticsHard

A patient's phenytoin dose is increased from 250 mg to 300 mg daily because their steady-state serum level of 12 mg/L (within the 10-20 mg/L range) was considered slightly low for seizure control. Two weeks later, their level is found to be 32 mg/L, well into the toxic range, despite the dose increase being only 20%. Which explanation best accounts for this disproportionate rise?

  1. APhenytoin absorption increases exponentially with dose, unrelated to metabolism
  2. BNear the saturation point of hepatic metabolising enzymes, a small percentage increase in dose can produce a much larger percentage increase in steady-state concentration because elimination capacity is nearly fixed
  3. CThe patient's phenytoin level was measured using an unreliable free-drug assay that overestimates total concentration
  4. DFirst-order elimination predicts exactly proportional changes, so a 20% dose rise should always produce roughly a 20% concentration rise, consistent with this case
  5. ERenal impairment developed acutely and is solely responsible for the rise, unrelated to hepatic saturation
Show answer and explanation

Answer: B Near the saturation point of hepatic metabolising enzymes, a small percentage increase in dose can produce a much larger percentage increase in steady-state concentration because elimination capacity is nearly fixed

The level rose from 12 to 32 mg/L, about 167%, after a dose increase of only 20%. This is the hallmark of saturable elimination, also called zero-order or Michaelis–Menten kinetics. At low concentrations, phenytoin is cleared by first-order kinetics, where a constant fraction is removed per unit time. Within the therapeutic range, the hepatic enzymes CYP2C9 and CYP2C19 approach their maximum capacity (Vmax). Elimination then becomes an almost fixed amount per day, so any extra dose accumulates. The steady-state level rises out of proportion, and the time taken to reach steady state also lengthens. In practice, change the dose in small steps and recheck the level after an adequate interval. The usual total range is 10–20 mg/L. Toxicity causes nystagmus, ataxia, slurred speech, drowsiness and confusion. Low albumin, renal failure and pregnancy increase the free fraction, so the total level can underestimate active drug. Drugs that inhibit CYP2C9, such as fluconazole or amiodarone, can also raise levels sharply.

Key clue
A modest 20% dose increase in phenytoin produced a much larger, disproportionate rise in steady-state serum concentration into the toxic range.
What it means
This pattern is characteristic of zero-order (saturation) kinetics, where elimination capacity is nearly maximal and cannot increase proportionally with dose.
What to do
Attribute the disproportionate rise to near-saturated hepatic metabolism limiting further increases in elimination rate.

Why the other options are less appropriate

  • A Oral absorption does not rise exponentially with dose. The disproportionate rise comes from saturation of hepatic metabolism.
  • C Nothing suggests an assay error. A large rise after a small dose increase is the classic effect of saturable metabolism.
  • D First-order kinetics would predict a rise of about 20%. The observed rise of about 167% contradicts this and shows non-linear kinetics.
  • E Phenytoin is cleared mainly by the liver. Renal impairment alters protein binding but does not explain this classic dose-related pattern.

Source: Phenytoin 100mg film-coated tablets - Summary of Product Characteristics (SmPC)

Question 5Malignant hyperthermiaHard

During anaesthesia with sevoflurane and suxamethonium, a patient develops rapidly rising end-tidal carbon dioxide, masseter rigidity, tachycardia, hyperkalaemia and increasing core temperature despite adequate ventilation. Which medicine is the specific immediate treatment?

  1. AIntravenous lipid emulsion
  2. BIntravenous sodium bicarbonate as sole definitive therapy
  3. CIntravenous calcium gluconate alone
  4. DIntravenous dantrolene
  5. EIntramuscular adrenaline
Show answer and explanation

Answer: D Intravenous dantrolene

This is malignant hyperthermia. A rise in end-tidal CO2 despite adequate ventilation, masseter rigidity, tachycardia, hyperkalaemia and a rising temperature after a volatile agent and suxamethonium all point to it. Most cases are caused by an autosomal dominant variant in RYR1 (less often CACNA1S). The trigger drugs cause uncontrolled calcium release from the sarcoplasmic reticulum, leading to sustained muscle contraction, high metabolism, rhabdomyolysis and acidosis. Dantrolene is the specific treatment. It blocks the ryanodine receptor and stops the calcium release. The Association of Anaesthetists and EMHG guidance gives 2.5 mg/kg IV straight away, then 1 mg/kg boluses as needed, up to 10 mg/kg. At the same time, stop the volatile agent, call for help, hyperventilate with 100% oxygen at high fresh gas flow, cool the patient actively, and treat the hyperkalaemia. Calcium channel blockers should not be given with dantrolene. Afterwards, refer the patient and family to the UK MH unit in Leeds for in vitro contracture testing and genetic testing.

Key clue
Volatile anaesthetic plus suxamethonium followed by rising carbon dioxide, rigidity and hyperthermia.
What it means
Uncontrolled ryanodine-receptor-mediated skeletal-muscle calcium release is causing malignant hyperthermia.
What to do
Give intravenous dantrolene immediately within the malignant-hyperthermia protocol.

Why the other options are less appropriate

  • A Lipid emulsion treats local anaesthetic toxicity. It has no effect on the muscle calcium release that drives malignant hyperthermia.
  • B Bicarbonate may help severe acidosis, but it does not stop the calcium release that drives this syndrome.
  • C Calcium can protect the heart from hyperkalaemia, but it does not treat malignant hyperthermia and may add to the calcium load.
  • E Adrenaline treats anaphylaxis. Here it would worsen the tachycardia and does nothing for the underlying cause.

Source: European Malignant Hyperthermia Group: Recognising and managing a malignant hyperthermia crisis

That is 5 of 346. Carry on with clinical pharmacology and therapeutics in the practice bank, with progress tracking, flashcards and timed sessions.

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Topics covered

Show all 326 clinical pharmacology and therapeutics topics
  • A negative genotype reduces one risk; it does not remove clinical vigilance
  • A paused withdrawal attempt without dose escalation
  • A positive HLA-B*15:02 result changes the treatment choice
  • A rise in HbA1c during statin treatment
  • ACE inhibitor and renal-function deterioration
  • ACE inhibitor pregnancy
  • ACE-inhibitor angioedema
  • ACE-inhibitor baseline tests
  • ACE-inhibitor cough
  • Acute illness
  • Acute laryngeal hereditary angioedema
  • Additional monitoring
  • Adverse drug reactions
  • Age-specific intravenous ondansetron dosing
  • Allergy documentation
  • Allergy investigation after a perioperative reaction
  • Allopurinol
  • Aminoglycoside monitoring
  • Aminoglycoside toxicity
  • Aminoglycosides
  • Amiodarone monitoring
  • Amiodarone pulmonary toxicity
  • Anaphylaxis
  • Anticholinergic burden
  • Anticoagulants/antiplatelets
  • Anticoagulation during breastfeeding
  • Anticoagulation reversal
  • Apparent failure of lipid-lowering treatment
  • Aspirin hypersensitivity
  • Asthma with nasal polyps before NSAID prescribing
  • Augmented renal clearance
  • Avoiding routine CK surveillance
  • Avoiding the non-selective NSAID class after suspected allergy
  • Azathioprine
  • Azathioprine and allopurinol
  • Azole inhibition of tacrolimus metabolism
  • Benzodiazepine-withdrawal adjuncts
  • Benzodiazepines
  • Beta-blocker overdose
  • Beta-blocker poisoning
  • Beta-lactams
  • Biased agonism
  • Binding interactions
  • Bioavailability
  • Black-triangle medicine reporting
  • Botulinum toxin
  • Bromocriptine
  • Calcium-channel blocker overdose
  • Calcium-channel blockers
  • Calculating the primary-prevention lipid response
  • Capacity-limited plasma-protein binding
  • Carbamazepine autoinduction
  • Carbamazepine poisoning despite multidose charcoal
  • Carbapenem-associated loss of valproate exposure
  • Carbimazole-associated pancreatitis and future exposure
  • Carbon monoxide
  • Clarithromycin–simvastatin interaction
  • Clearance
  • Clopidogrel and gastroprotection
  • Clozapine
  • Clozapine toxicity during serious infection
  • Clozapine-associated neutropenia
  • Codeine
  • Colchicine poisoning phases
  • Context-sensitive half-time
  • Corticosteroid sick-day rules
  • Corticosteroids
  • Cyanide
  • CYP2C19 poor metabolism and clopidogrel after PCI
  • Dabigatran capsule integrity in dysphagia
  • Dabigatran-associated life-threatening bleeding
  • Dapsone methaemoglobinaemia with G6PD deficiency
  • Dapsone-induced methaemoglobinaemia
  • Daptomycin
  • Deferasirox formulation conversion
  • Deferasirox-associated proximal tubular dysfunction
  • Dependence is not itself proof of addiction
  • Dependence risk and prescribing decisions
  • Dialysability
  • Digoxin
  • Digoxin immune Fab and serum digoxin assays
  • Digoxin toxicity
  • Distribution and extracorporeal drug removal
  • Do not initiate eculizumab during unresolved meningococcal infection
  • Do not make a blanket rule about long-term antibiotic prophylaxis
  • Do not turn HLA-A*31:01 association into universal screening
  • DOAC renal-function estimate
  • DOAC reversal
  • DOACs
  • Domperidone and phaeochromocytoma
  • Domperidone duration and dose
  • Dose-response
  • Doxycycline–polyvalent cation interaction
  • Dronedarone when atrial fibrillation becomes permanent
  • Drug-induced liver injury
  • Electronic prescribing systems
  • Elimination kinetics
  • Enterohepatic recycling
  • Enzyme induction
  • Enzyme-inducing medicines and contraception
  • Eplerenone and strong CYP3A4 inhibition
  • Exposure
  • Fever on C5 inhibition needs urgent assessment even without a rash
  • Fezolinetant
  • Finasteride 1 mg and new depressive symptoms
  • Finasteride 5 mg and psychiatric symptoms
  • Flip-flop kinetics
  • Flumazenil seizure risk
  • Fluoropyrimidines
  • Fluoroquinolone-associated tendinopathy
  • Fluoroquinolone-associated tendon injury
  • Food-dependent absorption of rivaroxaban 20 mg
  • Food-related loss of alendronate absorption
  • Fournier gangrene with an SGLT2 inhibitor
  • Free phenytoin in hypoalbuminaemia
  • Further lipid lowering after the secondary-prevention target
  • Gabapentin and aluminium–magnesium antacid timing
  • Gabapentinoid dose reductions
  • Gentamicin dose-weight selection
  • GLP-1 receptor agonist before anaesthesia
  • GLP-1 receptor agonist-associated pancreatitis
  • Glucarpidase for delayed high-dose methotrexate elimination
  • Glucocorticoid withdrawal
  • Grapefruit
  • Half-life
  • Heparin-induced thrombocytopenia
  • Hepatic clearance
  • Hepatic impairment and bioavailability
  • Herbal medicines
  • Hidden chlorhexidine exposure during procedures
  • High-extraction hepatic clearance
  • HLA-associated toxicity
  • HLA-B*15:02 and carbamazepine
  • HLA-B*58:01 and allopurinol
  • Hydrofluoric acid systemic toxicity
  • Hydroxychloroquine
  • Hydroxychloroquine with a macrolide
  • Immune-checkpoint inhibitor endocrinopathy
  • Interpreting phenytoin in hypoalbuminaemia
  • Interpreting PSA during established finasteride therapy
  • Intravenous-to-oral antibiotic switch
  • Investigating suspected drug allergy outside a specialist service
  • Ion trapping
  • Iron poisoning
  • Irreversible enzyme inhibition
  • Isolated gastrointestinal intolerance versus drug allergy
  • Isoniazid-induced refractory seizures
  • Isotretinoin
  • Ivabradine with a rate-limiting calcium-channel blocker
  • Kaftrio
  • Lamotrigine
  • Leflunomide washout
  • Levothyroxine–bile-acid sequestrant interaction
  • Linezolid
  • Linezolid-associated serotonin syndrome
  • Lithium
  • Lithium poisoning and post-dialysis rebound
  • Lithium toxicity
  • Liver-test monitoring after stable statin treatment
  • Loading and maintenance dosing
  • Loading dose
  • Loading dose calculation
  • Local anaesthetics
  • Local-anaesthetic systemic toxicity
  • Long-acting opioids
  • Macrolide interaction
  • Maintenance infusion calculation
  • Malignant hyperthermia
  • Marked triglyceridaemia without pancreatitis
  • Mechanism-based enzyme inhibition
  • Medicines reconciliation after admission
  • Mesalazine
  • Metabolism/elimination
  • Metformin and vitamin B12 deficiency
  • Metformin safety
  • Metformin-associated lactic acidosis
  • Metformin-associated lactic acidosis requiring dialysis
  • Methadone and benzodiazepines
  • Methotrexate
  • Methotrexate toxicity
  • Methotrexate–trimethoprim toxicity
  • Methylene blue limitations
  • Mild CK elevation before lipid treatment
  • Mild NSAID hypersensitivity and a selective alternative
  • Moderately raised transaminases before a statin
  • Modified-release opioids after surgery
  • Montelukast
  • Multiple antibiotic-class allergy labels restricting options
  • Mycophenolate
  • Neuroleptic malignant syndrome
  • New odynophagia during oral alendronate treatment
  • New pulmonary infiltrates during daptomycin treatment
  • Nitrates
  • Nitrofurantoin
  • Nitrofurantoin in renal impairment
  • No initial response versus recurrence after oral sumatriptan
  • Noncompetitive antagonism
  • Nonlinear kinetics
  • NSAIDs
  • One-to-one flutter conduction during flecainide treatment
  • Opioid and benzodiazepine co-prescribing
  • Opioid poisoning
  • Opioid switching
  • Opioid toxicity
  • Oral semaglutide formulation transition
  • Organophosphate poisoning
  • P-glycoprotein inhibition
  • Paracetamol
  • Paracetamol overdose
  • Partial agonism
  • Persistent ulceration associated with nicorandil
  • Persistently high CK before a statin
  • Pharmacogenomic prescribing
  • Planning conception while taking a statin
  • Posaconazole formulation substitution
  • Positive allosteric modulation
  • Pregabalin withdrawal
  • Pregnancy
  • Prescribing an unlicensed medicine
  • Preventing once-weekly methotrexate errors at transfer
  • Primary prevention beyond the QRISK age range
  • Primary-prevention dyslipidaemia with untreated hypothyroidism
  • Probenecid inhibition of tubular secretion
  • Prodrugs
  • Protein binding interactions
  • Proton pump inhibitors
  • Proton-pump inhibitor deprescribing
  • Pseudoephedrine
  • Psychological support during benzodiazepine withdrawal
  • QT prolongation
  • Rebound after abrupt tizanidine withdrawal
  • Receptor antagonism
  • Receptor down-regulation
  • Receptors
  • Recognising ivabradine-associated luminous phenomena
  • Recognising topical steroid withdrawal risk
  • Recurrent infections and a beta-lactam allergy label
  • Relative risk reduction
  • Renal dose adjustment
  • Renal impairment
  • Restarting lamotrigine after a prolonged interruption
  • Rifampicin and direct oral anticoagulants
  • Rifampicin interaction
  • Rifampicin–glucocorticoid interaction
  • Ritonavir markedly increases sildenafil exposure
  • Rivaroxaban administration beyond the stomach
  • Rizatriptan with propranolol
  • Rybelsus one-tablet rule
  • Salicylate poisoning
  • Saturation kinetics
  • Schild analysis
  • Screen before carbamazepine when risk ancestry is relevant
  • Secondary prevention while investigating a lipid cause
  • Self-limiting infection
  • Semaglutide
  • Separating allergy from other adverse effects
  • Serotonin syndrome
  • Severe NSAID reaction and a proposed COX-2 prescription
  • SGLT2 inhibitor interruption during major surgery
  • SGLT2 inhibitors
  • Short-acting beta-2 agonists
  • Short-half-life benzodiazepine withdrawal
  • SLCO1B1 poor function and simvastatin
  • Small early creatinine rise on dronedarone
  • Smoking cessation and clozapine toxicity
  • Sofosbuvir-containing treatment after amiodarone exposure
  • Specialist follow-up after a severe delayed reaction
  • Staggered paracetamol overdose
  • Starting spironolactone
  • Starting valproate in a patient younger than 55
  • Statin dose escalation in advanced CKD
  • Statin interactions
  • Statin-associated muscle toxicity
  • Stewardship
  • Structured medication review
  • Sugammadex and hormonal contraception
  • Sulfonylureas
  • Sumatriptan after recent MAO inhibitor discontinuation
  • Suspected local-anaesthetic allergy before an essential procedure
  • Symptomatic hyperammonaemia with normal liver tests
  • Tacrolimus
  • Taking over a dependence-forming prescription
  • Target-mediated drug disposition
  • Teratogenic medicines
  • Testing suspected statin intolerance
  • Theophylline poisoning and extracorporeal treatment
  • Therapeutic drug monitoring
  • Therapeutic index
  • Therapeutic monitoring
  • Thiopurines
  • Thyroid testing in the baseline statin assessment
  • Time-to-event analysis
  • Tirzepatide
  • Tizanidine and ciprofloxacin interaction
  • Tolerance
  • Topical nasal decongestants
  • Topiramate for epilepsy and pregnancy
  • Topiramate for migraine in pregnancy
  • Toxic alcohol poisoning
  • Transdermal fentanyl
  • Tricyclic antidepressant overdose
  • Tricyclic-antidepressant poisoning
  • Triglycerides and an apparently reassuring risk score
  • Trimethoprim-associated hyperkalaemia
  • Type 1 diabetes and statin eligibility in a younger adult
  • UGT1A1 poor metabolism and irinotecan
  • Unknown allergy history in an unconscious patient
  • Updating records after allergy is excluded
  • Urgent harm as an exception to a slow medication taper
  • Urgent treatment may outweigh waiting for the full vaccine interval
  • Valproate
  • Valproate alters lamotrigine escalation
  • Valproate and reproductive risk
  • Valproate poisoning and haemodialysis
  • Valproate pregnancy prevention
  • Valproate-associated hyperammonaemic encephalopathy
  • Vancomycin exposure monitoring
  • Vancomycin monitoring
  • Very severe triglyceridaemia and referral
  • Warfarin
  • Warfarin and amiodarone
  • Warfarin and tramadol
  • Why tryptase samples need their collection times
  • Withdrawal symptoms or relapse
  • Withdrawal/deprescribing
  • Yellow Card

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