PLAB 1 (UKMLA AKT) mental health questions

When switching between most SSRIs, including from citalopram to sertraline, a cross-taper approach is recommended: the dose of citalopram is gradually reduced while sertraline is introduced and gradually increased over 1-2 weeks, as both drugs have relatively low risk of serious interaction with each other. This minimises the risk of discontinuation symptoms from citalopram while allowing therapeutic sertraline levels to build. A washout period is not required between these two SSRIs, unlike when switching to or from drugs such as fluoxetine or MAOIs, which require longer gaps due to prolonged half-lives or interaction risk.

• A. Continuing citalopram indefinitely at low dose alongside sertraline is unnecessary and increases the risk of combined serotonergic adverse effects.
• B. A 2-week washout is unnecessary between these two SSRIs and would prolong the patient's depressive symptoms without benefit.
• D. Starting a new antidepressant at full dose while continuing the first unchanged risks additive serotonergic effects and is not standard practice.
• E. Abrupt cessation of citalopram risks discontinuation symptoms rather than a smooth transition to the new antidepressant.

This patient has failed to respond to both high-intensity psychological therapy and an adequate dose and duration of an SSRI, meeting criteria for treatment-resistant depression. NICE guidance recommends referral to secondary care mental health services for specialist assessment and consideration of augmentation strategies (e.g. lithium, antipsychotic augmentation) or combination treatment, as these decisions require specialist monitoring. Starting augmentation agents such as lithium in primary care is not appropriate due to the need for specialist initiation and monitoring. There is no indication here of risk to self that would warrant emergency assessment or detention.

• A. Switching antidepressant class alone is insufficient after failure of both psychological therapy and an adequate SSRI trial; specialist input is needed.
• B. There is no evidence of risk to self or others or of a mental disorder requiring detention; admission under the Act is not indicated.
• D. Lithium augmentation requires specialist initiation and monitoring (renal and thyroid function, levels) and is not started in primary care.
• E. The dose and duration have already been adequate; continuing unchanged treatment with no response is not appropriate.

Puerperal (postpartum) psychosis is a psychiatric emergency that typically presents within the first 2 weeks after delivery, often abruptly, with rapidly fluctuating mood, agitation, insomnia, and psychotic features such as paranoid delusions or hallucinations, as seen here. Baby blues is a much milder, self-limiting tearfulness and emotional lability peaking around day 3-5 and resolving within 2 weeks without psychotic features. Postnatal depression typically develops over the first few weeks to months with low mood, anhedonia and fatigue, not acute psychosis. This presentation requires urgent psychiatric assessment, ideally with admission to a mother and baby unit.

• A. Postnatal depression presents with persistent low mood and anhedonia over weeks, not acute psychotic symptoms within days of delivery.
• B. Baby blues causes mild tearfulness and mood lability, not paranoid delusions or agitation of this severity.
• C. GAD involves chronic worry rather than acute paranoid delusions and agitation in the immediate postpartum period.
• D. The presence of delusional beliefs and agitation is pathological, not a normal adjustment to new parenthood.

NICE recommends a stepped-care approach for GAD: step 1 is identification and education, step 2 is low-intensity psychological interventions (individual non-facilitated or facilitated self-help, psychoeducational groups), step 3 is high-intensity psychological intervention (CBT or applied relaxation) or drug treatment when step 2 has failed, and step 4 is referral to specialist services for severe, treatment-refractory GAD with significant functional impairment. Since this patient has not improved after step 2 low-intensity interventions, he should move to step 3, offered a choice between high-intensity CBT and drug treatment, typically an SSRI such as sertraline. Benzodiazepines are not recommended for routine long-term management of GAD.

• B. Benzodiazepines are not recommended for the routine management of GAD due to dependence risk and lack of long-term efficacy.
• C. Specialist referral (step 4) is reserved for very severe GAD with significant impairment unresponsive to step 3 interventions, which has not yet been tried here.
• D. Repeating the same step with a different provider is not indicated once a low-intensity intervention has failed; the patient should be stepped up, not laterally moved.
• E. An SSRI is one acceptable step-3 option but should be offered alongside, not instead of, the choice of high-intensity CBT; naming the drug directly skips the stepped choice NICE recommends be offered to the patient.

Panic disorder is characterised by recurrent, unexpected panic attacks consisting of a rapid surge of intense fear with physical symptoms such as palpitations, sweating, trembling and chest discomfort, peaking within minutes and accompanied by fear of dying or losing control, followed by persistent worry about future attacks. The normal ECG and troponin, together with the episodic, self-limiting nature and interictal anxiety about recurrence, support panic disorder over a cardiac cause. GAD involves chronic diffuse worry rather than discrete attacks, and the episodic pattern here with normal cardiac investigations argues against an acute coronary syndrome.

• A. GAD presents with persistent, diffuse worry rather than discrete, sudden attacks of intense fear and physical symptoms.
• B. Somatic symptom disorder involves persistent distressing physical symptoms without this characteristic abrupt panic attack pattern and fear of dying.
• D. Social anxiety disorder is triggered specifically by social or performance situations, not unexpected attacks occurring at other times.
• E. Unstable angina is excluded by the normal ECG and troponin and by the pattern of self-limiting episodes with interictal wellness.

Social anxiety disorder is characterised by marked, persistent fear of social or performance situations in which the person is exposed to possible scrutiny and fears acting in a way that will be humiliating or embarrassing, leading to avoidance of a range of social contexts such as this patient's avoidance of meetings, restaurants and parties. Specific phobia involves fear restricted to a particular object or situation (e.g. animals, heights), which this patient explicitly denies. Agoraphobia centres on fear of situations from which escape might be difficult, such as crowds or open spaces, rather than fear of negative social judgement specifically.

• A. GAD involves diffuse worry about multiple life domains rather than fear focused specifically on social evaluation.
• B. Specific phobia is limited to a discrete object or situation; this patient's fear spans multiple social contexts and centres on fear of judgement.
• D. Avoidant personality disorder is a pervasive, lifelong pattern affecting broader relationships and self-image, not a discrete anxiety disorder diagnosis fitting this presentation best as a first-line diagnosis.
• E. Agoraphobia involves fear of being unable to escape or get help, typically in crowded or open spaces, rather than fear of social scrutiny.

Obsessions are recurrent, intrusive, unwanted thoughts, images or urges that cause marked anxiety and are recognised by the patient as excessive or irrational, as with this patient's contamination fears. Compulsions are the repetitive behaviours or mental acts, such as washing or checking, performed to reduce the anxiety generated by the obsessions. First-line pharmacological treatment for OCD is an SSRI (e.g. fluoxetine, sertraline), typically requiring a higher dose and a longer trial (up to 12 weeks) than for depression before response is judged. Delusions and hallucinations are features of psychotic disorders, and the patient's insight into the irrationality of her thoughts distinguishes OCD from psychosis.

• A. Delusions are fixed, false beliefs held without insight; this patient recognises her thoughts are excessive, indicating preserved insight.
• B. Hallucinations are perceptions in the absence of a stimulus and are not a feature of this patient's presentation.
• D. Compulsions are the repetitive behaviours (washing, checking) performed in response to obsessions, not the intrusive thoughts themselves.
• E. Phobic stimuli are external objects or situations that trigger fear in specific phobia, not internally generated intrusive thoughts.

This patient's symptoms of intrusive re-experiencing, avoidance, hyperarousal and sleep disturbance persisting for more than 4 weeks after a traumatic event causing significant distress meet criteria for post-traumatic stress disorder (PTSD), as acute stress reaction/disorder is diagnosed only within the first 4 weeks. NICE recommends trauma-focused CBT (or EMDR as an alternative) as first-line treatment for PTSD, and this should be offered to all patients with a diagnosis of PTSD regardless of the time since the trauma. Drug treatment such as an SSRI is reserved for when psychological therapy is declined, ineffective or unavailable, and benzodiazepines are not recommended due to risk of dependence and lack of evidence for efficacy in PTSD.

• A. Symptoms have persisted beyond 4 weeks and are causing significant distress, meeting PTSD criteria; this warrants active treatment, not simple reassurance and delayed review.
• B. Inpatient admission is not indicated in the absence of risk to self or others or severe functional collapse; outpatient trauma-focused therapy is appropriate.
• C. Benzodiazepines are not recommended in PTSD due to dependence risk and lack of proven benefit for core symptoms.
• D. Trauma-focused psychological therapy is first-line; drug treatment is reserved for when therapy is declined, ineffective or unavailable.

Acute stress reaction occurs within hours to days of an exceptionally threatening or traumatic event and resolves within one month; this woman is two weeks post-trauma with typical hyperarousal and intrusive symptoms, fitting this timeframe. PTSD requires symptoms to persist beyond one month. Adjustment disorder follows an identifiable non-catastrophic stressor (such as divorce or job loss) rather than a life-threatening trauma. The distinction matters because management of acute stress reaction is supportive, with trauma-focused CBT reserved for PTSD if symptoms persist.

• A. Normal grief does not typically present with marked hyperarousal and intrusive re-experiencing this early.
• B. Adjustment disorder is triggered by non-traumatic stressors, not a life-threatening event like this.
• C. PTSD cannot be diagnosed until symptoms have persisted for at least one month.
• E. Generalised anxiety disorder requires persistent, free-floating anxiety unrelated to a specific traumatic trigger.

Benzodiazepines are effective for rapid relief of acute anxiety but carry a significant risk of tolerance and dependence with continued use, so UK guidance recommends restricting prescriptions to the lowest effective dose for the shortest time, typically no more than 2–4 weeks. Longer courses should be avoided even in bereavement-related anxiety. If symptoms persist beyond this, alternative strategies such as CBT or an SSRI should be considered rather than continuing benzodiazepines. Clear time-limiting at the point of prescribing helps prevent inadvertent long-term use and withdrawal difficulties.

• A. Open-ended prescribing without a review date substantially increases the risk of dependence.
• B. Family history does not determine whether short-term benzodiazepine use is appropriate.
• C. Citalopram is not indicated as an immediate measure for acute short-term anxiety and takes weeks to act; it is not the issue being tested here.
• E. Six months of continuous use is far longer than recommended and risks significant dependence.

Suspected first-episode psychosis requires urgent referral to an early intervention in psychosis (EIP) service, with NICE guidance recommending assessment within two weeks of referral, as early treatment improves long-term outcomes. Antipsychotics should be initiated and monitored by secondary care specialists as part of a comprehensive assessment, not started empirically in primary care. Delaying referral for routine review risks prolonging untreated psychosis, which is associated with worse prognosis. This patient has no evidence of substance misuse, so a drug service referral is not the priority.

• A. Routine referral is too slow; EIP referral should prompt assessment within two weeks.
• B. There is no history or evidence suggesting substance misuse is driving his symptoms.
• C. Antipsychotic initiation in suspected first-episode psychosis should be managed by secondary care EIP services, not started unsupervised in primary care.
• E. Watchful waiting delays treatment and risks a longer duration of untreated psychosis.

Third-person running commentary voices and thought broadcasting are both classical Schneiderian first-rank symptoms strongly associated with schizophrenia when occurring in clear consciousness without an organic or mood cause. First-rank symptoms also include thought insertion, thought withdrawal, delusional perception, and somatic passivity. Their presence supports a diagnosis of schizophrenia once substance use and mood disorder have been excluded, as in this patient. These symptoms reflect disturbances in the sense of self and ownership of thoughts and actions.

• A. Capgras delusion is the belief that a familiar person has been replaced by an impostor, not described here.
• C. Hypnagogic hallucinations occur during the transition to sleep and are not described here.
• D. Formal thought disorder refers to disorganised speech and thinking, not the specific hallucination and broadcasting phenomena described.
• E. The patient denies low mood, making mood-congruent delusions irrelevant.

An oral atypical (second-generation) antipsychotic such as risperidone, olanzapine or aripiprazole is first-line in new-onset psychosis because these agents have a lower risk of extrapyramidal side effects compared with typical antipsychotics, improving tolerability and adherence. Clozapine is reserved for treatment-resistant schizophrenia after at least two adequate trials of other antipsychotics have failed, not first-line use. Typical antipsychotics like haloperidol and chlorpromazine carry a higher risk of extrapyramidal symptoms and are not preferred initial choices. Depot formulations are generally considered later, for relapse prevention or adherence issues, rather than at first presentation.

• A. Chlorpromazine, also typical, has a similarly higher side-effect burden and is not preferred as initial therapy.
• B. Depot antipsychotics are not first-line for a newly diagnosed, treatment-naive patient who has not yet demonstrated adherence issues.
• C. Clozapine is reserved for treatment resistance after two antipsychotics have failed, due to its agranulocytosis risk and monitoring requirements.
• E. Haloperidol, a typical antipsychotic, carries a higher risk of extrapyramidal side effects and is not first-line.

Clozapine is indicated for treatment-resistant schizophrenia, defined as failure to respond adequately to at least two different antipsychotics (at least one being atypical), each given at an adequate dose for an adequate trial period with confirmed adherence. This patient meets that criterion, having failed two documented antipsychotic trials. Clozapine has superior efficacy in treatment-resistant disease but requires registration with a monitoring service and regular blood count checks due to agranulocytosis risk. Trying further standard antipsychotics or antipsychotic combinations is not supported by evidence once resistance criteria are met.

• A. Trialling a third standard antipsychotic is not recommended once treatment-resistance criteria have been met; clozapine should be offered instead.
• C. Exceeding the licensed maximum dose increases toxicity risk without established benefit and is not standard practice.
• D. Switching to a typical depot does not address treatment resistance and is not the guideline-recommended next step.
• E. Antipsychotic polypharmacy lacks strong evidence and increases side-effect burden without proven benefit over clozapine in resistant disease.

This presentation of hyperthermia, lead-pipe rigidity, autonomic instability, altered consciousness and markedly raised creatine kinase after antipsychotic use is characteristic of neuroleptic malignant syndrome, a medical emergency. Immediate management involves stopping the offending antipsychotic, aggressive intravenous fluid rehydration to protect renal function from rhabdomyolysis, and transfer to a setting with intensive monitoring, as supportive care with cooling and correction of electrolytes is essential. Dantrolene or bromocriptine may be used in severe or refractory cases under specialist guidance. Continuing or switching antipsychotics without first stopping the causative drug risks worsening the syndrome and is inappropriate.

• A. Lorazepam alone without stopping the causative drug and providing supportive care is inadequate, and discharge would be unsafe given his instability.
• C. Continuing the causative antipsychotic, even at a reduced dose, risks worsening neuroleptic malignant syndrome and is dangerous.
• D. Oral paracetamol does not address the underlying mechanism and ward observation alone is insufficient for this emergency.
• E. Starting another antipsychotic without first stopping haloperidol and stabilising the patient would worsen the clinical picture.

Acute dystonia typically occurs within hours to days of starting or increasing a typical antipsychotic and presents with sustained, involuntary muscle contractions such as torticollis, trismus or oculogyric crisis. It results from dopamine D2 receptor blockade in the nigrostriatal pathway and is treated promptly with an anticholinergic such as procyclidine. Normal vital signs and preserved consciousness distinguish this from neuroleptic malignant syndrome or a seizure.

• A. A seizure would cause loss of consciousness and typically tongue biting or incontinence, neither present here.
• B. Akathisia causes subjective inner restlessness and an inability to sit still, not sustained muscle contraction.
• C. Tardive dyskinesia develops after months to years of treatment and causes choreoathetoid movements, not acute sustained spasm.
• D. Neuroleptic malignant syndrome features fever, rigidity and autonomic instability, which are absent here.

Risperidone is a potent D2 receptor antagonist that readily crosses into the tuberoinfundibular pathway, removing dopamine's inhibitory effect on the pituitary and raising prolactin. Elevated prolactin causes amenorrhoea, galactorrhoea and reduced libido through suppression of gonadotropin-releasing hormone. Management includes checking a serum prolactin level, excluding pregnancy, and considering switching to a prolactin-sparing antipsychotic such as aripiprazole if symptomatic.

• A. Premature ovarian insufficiency causes amenorrhoea but not galactorrhoea, and would not explain this temporal link to risperidone.
• B. PCOS causes irregular periods and hirsutism but does not typically cause galactorrhoea.
• C. Hypothyroidism can raise prolactin secondarily via TRH but the history of starting risperidone makes drug-induced hyperprolactinaemia far more likely.
• E. Pregnancy has been excluded and would not account for the temporal relationship with starting risperidone.

Delusional disorder is characterised by one or more fixed, non-bizarre delusions persisting for at least three months (ICD-11) in the absence of hallucinations, thought disorder, or significant deterioration in functioning, with the delusion typically being well-organised and encapsulated as in this persecutory belief. Her preserved occupational and social functioning and absence of hallucinations or disorganised speech argue against schizophrenia. The circumscribed nature of the belief, with otherwise intact mental state, is the key distinguishing feature.

• A. Schizoaffective disorder requires a concurrent mood episode alongside psychotic symptoms, which is not described here.
• C. There is no description of depressive symptoms, so adding a depressive qualifier is unsupported by the history.
• D. Schizophrenia requires additional features such as hallucinations, thought disorder or negative symptoms with functional decline, none of which are present.
• E. Schizotypal personality disorder involves eccentric beliefs and social anxiety from an early age, not a single fixed delusion.

Mania is diagnosed when elevated or irritable mood with increased energy persists for at least one week and is severe enough to cause marked impairment in functioning or to require hospitalisation, often accompanied by psychotic features such as grandiose delusions, as seen here with her belief of being a prime ministerial advisor. Hypomania is a milder, shorter form (at least 4 days) without psychosis or severe functional impairment. The duration of 10 days, grandiose delusion, and reckless overspending indicate mania rather than hypomania.

• B. Generalised anxiety disorder does not explain grandiosity, decreased need for sleep or psychotic delusions.
• C. A mixed episode requires concurrent depressive symptoms, which are not described.
• D. Hypomania lacks psychotic features and does not cause the severe functional impairment seen here, such as attempting to enter a government building.
• E. An acute stress reaction follows an identifiable traumatic stressor and resolves within hours to days, which does not fit this presentation.

Before starting lithium, baseline renal function (urea and electrolytes, estimated glomerular filtration rate) and thyroid function tests are mandatory, as lithium can cause nephrogenic diabetes insipidus, chronic kidney disease and hypothyroidism with long-term use. Calcium should also be checked as lithium is associated with hyperparathyroidism, and an ECG is recommended in patients with cardiovascular risk factors because lithium can affect cardiac conduction. These baseline results allow monitoring for lithium-induced organ toxicity over time.

• A. Prolactin and pregnancy testing are not part of the standard lithium baseline panel, though pregnancy status should be discussed separately.
• B. Fasting glucose and lipids are relevant to antipsychotic monitoring, not specifically required before starting lithium.
• D. Liver function and full blood count are not the key baseline tests specifically required before starting lithium.
• E. Chest X-ray and EEG are not part of routine baseline lithium monitoring.

Lithium has a narrow therapeutic index, and dehydration from vomiting and diarrhoea reduces renal clearance, allowing lithium to accumulate to toxic levels. Features of lithium toxicity include coarse tremor, ataxia, dysarthria, blurred vision, confusion and, in severe cases, seizures or coma. Management requires stopping lithium, checking a serum lithium level urgently, and giving intravenous fluids, with haemodialysis considered in severe toxicity. Other common precipitants include NSAIDs, ACE inhibitors, diuretics and reduced sodium intake.

• A. Serotonin syndrome occurs with serotonergic drugs and features hyperthermia, clonus and hyperreflexia, not the clear dehydration-triggered picture here.
• C. Hepatic encephalopathy would require evidence of liver disease, which is not suggested by this history.
• D. Neuroleptic malignant syndrome is linked to antipsychotic use and presents with fever and rigidity, which are not the dominant features here.
• E. There is no history of alcohol use disorder or recent cessation of drinking to suggest withdrawal.

Sodium valproate is highly teratogenic, causing neural tube defects and other congenital malformations, and is associated with neurodevelopmental disorders in up to 30-40% of children exposed in utero. The MHRA/GMC Pregnancy Prevention Programme states valproate must not be prescribed to women of childbearing potential unless other treatments are ineffective or not tolerated, and only under specialist supervision with highly effective contraception. Since this patient is actively planning pregnancy, she should be referred to psychiatry for a planned, gradual switch to a safer alternative before conception, rather than an abrupt change. Decisions about stopping or switching mood stabilisers in bipolar disorder should not be made in primary care alone given relapse risk.

• A. Folic acid does not mitigate valproate's teratogenic effects enough to make continuation safe.
• B. Abrupt cessation risks acute relapse and lithium should not be started without specialist planning.
• D. Continuing valproate unchanged exposes a planned pregnancy to major teratogenic risk.
• E. Halving the dose still carries significant teratogenic risk and does not address the underlying issue.

Lithium is the first-line maintenance treatment for bipolar affective disorder according to NICE guidance (CG185/NG table equivalents), as it has the strongest evidence base for preventing relapse of both manic and depressive episodes. It requires baseline and ongoing monitoring of renal and thyroid function and serum lithium levels due to its narrow therapeutic index. Valproate is an alternative but is avoided in women of childbearing potential and is not first-line in men without contraindication to lithium. Antidepressants such as fluoxetine are not used as monotherapy maintenance treatment in bipolar disorder due to the risk of triggering mania. Benzodiazepines have no role in long-term relapse prevention.

• A. Valproate is a second-line option, used mainly when lithium is contraindicated or ineffective.
• B. Antidepressant monotherapy risks precipitating a manic switch and is not used for maintenance.
• C. Chlordiazepoxide is used for alcohol withdrawal, not for bipolar maintenance treatment.
• E. Diazepam is used short-term for acute agitation, not for long-term relapse prevention.

Emotionally unstable (borderline) personality disorder is characterised by a pervasive pattern, beginning in adolescence or early adulthood, of unstable relationships, identity disturbance, affective instability, chronic emptiness, impulsivity, and recurrent self-harm often triggered by interpersonal stress. The chronic, pervasive, trait-like pattern starting in youth distinguishes it from bipolar disorder, in which mood episodes are more episodic and sustained over days to weeks rather than hours in response to triggers. Histrionic personality disorder features attention-seeking and excessive emotionality but lacks the chronic self-harm and abandonment fears seen here. There is no clear history of a precipitating trauma or amnesia/identity fragmentation to support PTSD or dissociative identity disorder.

• A. There is no described traumatic event or re-experiencing symptoms to support PTSD.
• B. Rapid cycling bipolar disorder involves sustained mood episodes, not moment-to-moment reactivity to interpersonal triggers.
• C. Histrionic personality disorder centres on attention-seeking behaviour rather than fear of abandonment and chronic self-harm.
• E. Dissociative identity disorder requires distinct identity states, which are not described here.

Anorexia nervosa is diagnosed by restriction of energy intake leading to significantly low body weight, intense fear of weight gain or persistent behaviour that interferes with weight gain, and a disturbance in how body weight is experienced. This patient has a very low BMI (15.1 kg/m²), bradycardia, hypotension, amenorrhoea, and lanugo hair, all recognised physical risk markers of starvation and important for assessing the severity and urgency of physical risk. Bulimia nervosa is characterised by binge-purge cycles typically with normal or near-normal weight, which does not fit this low-BMI presentation. ARFID involves food avoidance without the body image disturbance or fear of weight gain central to anorexia nervosa.

• A. ARFID lacks the fear of weight gain and body image disturbance central to this presentation.
• C. Bulimia nervosa typically occurs at normal or near-normal body weight with binge-purge cycles, not severe underweight.
• D. Depression can cause weight loss but does not explain the fear of weight gain and lanugo hair.
• E. Hyperthyroidism causes weight loss with tachycardia, not the bradycardia seen here.

Refeeding syndrome occurs when carbohydrate reintroduction after prolonged starvation triggers a surge in insulin secretion, which drives potassium, magnesium, and phosphate into cells along with glucose, causing severe extracellular hypokalaemia, hypomagnesaemia, and hypophosphataemia. This can precipitate cardiac arrhythmias, respiratory failure, and neurological disturbance, as suggested by this patient's weakness and dyspnoea. NICE guidance recommends starting nutritional support at a cautious calorie level in high-risk patients and correcting electrolytes with monitoring, alongside thiamine supplementation, to prevent this complication. The mechanism is intracellular electrolyte shift rather than direct organ toxicity, pancreatic injury, or adrenal pathology.

• A. Adrenal insufficiency is not a recognised cause of this electrolyte pattern in refeeding.
• B. Nasogastric feed is not directly nephrotoxic; the electrolyte shifts occur due to insulin-mediated cellular uptake.
• C. Acute pancreatitis is not the typical mechanism of refeeding syndrome and is not supported by this presentation.
• E. Rhabdomyolysis would cause elevated potassium and phosphate from cell breakdown, not the low levels seen here.

Bulimia nervosa is characterised by recurrent binge eating episodes with loss of control, followed by compensatory behaviours such as self-induced vomiting, occurring at least weekly for three months, in a patient who is typically of normal or near-normal body weight. Repeated vomiting causes a hypokalaemic, hypochloraemic metabolic alkalosis (raised bicarbonate) due to loss of gastric acid and potassium, and dental enamel erosion from recurrent exposure to stomach acid. Anorexia nervosa binge-purge subtype requires a significantly low body weight, which is absent here given a BMI of 22 kg/m². Binge eating disorder lacks compensatory purging behaviour.

• A. Anorexia nervosa binge-purge subtype requires a significantly low BMI, which this patient does not have.
• B. Binge eating disorder does not include compensatory vomiting, which is present here.
• C. Pica involves eating non-food substances, not binge eating and purging.
• E. Rumination disorder involves effortless regurgitation of recently eaten food, not purposeful vomiting after binges.

This patient meets several MARSIPAN (Management of Really Sick Patients with Anorexia Nervosa) criteria for high physical risk requiring urgent hospital admission: a very low BMI (below 13 kg/m²), marked bradycardia (heart rate below 40 beats per minute), hypotension, and hypothermia (core temperature below 35°C). These findings indicate a high risk of sudden cardiac death and electrolyte disturbance, requiring immediate medical stabilisation in an acute hospital setting rather than continued community management. Outpatient measures such as increased dietitian review, supplementation, psychological therapy, or community-supervised feeding are inappropriate given the severity of physiological compromise.

• B. Outpatient review is insufficient given the severe bradycardia, hypotension, and hypothermia indicating high medical risk.
• C. Oral supplementation alone does not address the acute cardiovascular instability present.
• D. Nasogastric feeding at home is unsafe given the degree of cardiovascular compromise; she needs inpatient monitoring.
• E. Psychological therapy is not appropriate while the patient is at acute physical risk requiring medical stabilisation.

Chronic alcohol use enhances inhibitory GABA-A receptor activity and suppresses excitatory NMDA glutamate receptor activity; abrupt cessation removes this depressant effect, unmasking a hyperexcitable, up-regulated glutamatergic and down-regulated GABAergic state. This produces a predictable timeline: autonomic hyperactivity and tremor within 6-24 hours, seizures around 24-48 hours, and delirium tremens, with confusion, hallucinations, autonomic instability, and fever, typically peaking at 48-72 hours after the last drink. This mechanism, rather than direct acetaldehyde toxicity, thiamine deficiency (which causes Wernicke's encephalopathy with ataxia, ophthalmoplegia, and confusion rather than this classic DT picture), hepatic encephalopathy, or hypoglycaemia, explains the described progression.

• A. There is no mention of liver failure or raised ammonia to support hepatic encephalopathy here.
• B. Thiamine deficiency causes Wernicke's encephalopathy, a distinct syndrome with ataxia and ophthalmoplegia, not this withdrawal timeline.
• D. Hypoglycaemia is not described and does not account for the autonomic and hallucinatory features seen.
• E. Acetaldehyde toxicity is not the mechanism of withdrawal-related CNS hyperexcitability.

In uncomplicated alcohol withdrawal with normal liver function, a fixed-dose reducing regimen of oral chlordiazepoxide over 5-7 days is standard, with symptom-triggered additional doses (using a tool such as CIWA-Ar) available for breakthrough symptoms. This approach prevents seizures and delirium tremens while minimising over-sedation. Chlordiazepoxide is preferred over shorter-acting benzodiazepines because its longer half-life gives a smoother withdrawal course. Liver impairment would favour a shorter-acting agent such as lorazepam instead.

• B. Intravenous chlordiazepoxide is not standard practice; oral dosing is used for routine withdrawal management.
• C. Diazepam loading is used in some settings but is not routine UK ward practice for uncomplicated withdrawal, and stopping after symptom resolution without a planned taper risks rebound withdrawal.
• D. Chlorpromazine lowers seizure threshold and is not appropriate as first-line treatment for alcohol withdrawal.
• E. A single stat dose and observation alone is inadequate; alcohol withdrawal requires a structured multi-day regimen to prevent progression to seizures or delirium tremens.

This patient has the classic triad of Wernicke's encephalopathy: confusion, ophthalmoplegia (nystagmus and lateral rectus palsy) and ataxia, caused by thiamine deficiency in chronic alcohol misuse. Giving glucose before thiamine can precipitate or worsen Wernicke's encephalopathy because glucose metabolism consumes remaining thiamine stores, so intravenous thiamine (e.g. Pabrinex) must be given first or alongside glucose, never after. Oral thiamine is insufficient in this acute emergency and has poor bioavailability. Prompt treatment is essential to prevent progression to irreversible Korsakoff syndrome.

• A. Imaging should not delay emergency thiamine replacement; this is a clinical diagnosis requiring immediate treatment.
• B. Magnesium may be co-administered as a cofactor but thiamine replacement is the immediate priority, not magnesium alone.
• C. Giving dextrose before thiamine risks precipitating or worsening Wernicke's encephalopathy by depleting remaining thiamine reserves.
• D. Oral thiamine has poor bioavailability and is inadequate for treating an acute presentation of Wernicke's encephalopathy.

NICE recommends AUDIT as the preferred screening tool for identifying hazardous and harmful alcohol use in primary care, as it assesses quantity, frequency, dependence features and alcohol-related problems across 10 questions, giving a score that stratifies risk. CAGE is a shorter screening tool but is less sensitive for identifying hazardous (non-dependent) drinking and focuses more on dependence features. HADS, PHQ-9 and GAD-7 are validated tools for depression and anxiety, not alcohol misuse.

• A. CAGE is a quicker screen weighted towards detecting dependence rather than the full spectrum of hazardous and harmful drinking that NICE recommends AUDIT for in primary care.
• B. PHQ-9 is a depression severity screening tool, unrelated to alcohol use.
• C. HADS screens for anxiety and depression symptoms, not alcohol consumption.
• D. GAD-7 screens for generalised anxiety disorder, not alcohol misuse.

The combination of respiratory depression, pinpoint (miotic) pupils and reduced consciousness is classic for opioid overdose, and naloxone is the specific antidote that rapidly reverses respiratory depression by competitively antagonising opioid receptors. It should be given promptly by intramuscular or intravenous route alongside airway support and oxygen, as delay risks hypoxic brain injury or death. Flumazenil reverses benzodiazepines, not opioids, and is not indicated here. A pulse should be checked, and if present, chest compressions are not the priority.

• A. Chest compressions are only indicated if the patient is pulseless; the priority here is reversing respiratory depression with naloxone.
• B. Flumazenil reverses benzodiazepine, not opioid, toxicity and would not address this presentation.
• C. Intubation may be needed if naloxone fails to restore adequate ventilation, but naloxone should be trialled first as it is rapid and non-invasive.
• E. Oxygen alone does not address the underlying opioid-induced respiratory depression and delaying antidote treatment risks deterioration.

This presentation, mydriasis (dilated pupils), piloerection, sweating, gastrointestinal symptoms and myalgia occurring after a period of abstinence in an opioid-dependent patient, is characteristic of opioid withdrawal. This contrasts with opioid intoxication, which presents with miosis, respiratory depression and sedation rather than agitation and dilated pupils. The normal respiratory rate and oxygen saturation here are inconsistent with opioid toxicity. Management typically involves symptomatic relief and consideration of opioid substitution therapy.

• A. Alcohol withdrawal can cause autonomic hyperactivity but would not explain piloerection and is not supported by the history of heroin use.
• B. Benzodiazepine intoxication causes sedation rather than agitation and gastrointestinal symptoms described here.
• D. Opioid intoxication causes miosis, sedation and respiratory depression, the opposite of this patient's dilated pupils and agitation.
• E. Stimulant intoxication can cause mydriasis and agitation but does not typically cause piloerection, diarrhoea and the clear temporal relationship to opioid cessation seen here.

Long-term benzodiazepine use leads to physical dependence, and abrupt cessation risks withdrawal symptoms including rebound anxiety, insomnia, tremor and, in severe cases, seizures. The recommended approach is a gradual dose reduction, typically in decrements of around one-eighth of the daily dose every fortnight, adjusted according to the severity of withdrawal symptoms, often over weeks to months. This can usually be managed in primary care without hospital admission unless withdrawal is severe or complicated. Switching to a shorter-acting benzodiazepine and stopping abruptly would worsen withdrawal rather than prevent it.

• A. Routine benzodiazepine withdrawal in a patient without complicating factors does not require emergency inpatient admission and can be managed in primary care.
• B. Abrupt discontinuation after long-term use risks significant withdrawal symptoms including seizures and should be avoided.
• C. Indefinite continuation is not appropriate management; a structured taper allows safe discontinuation.
• E. Switching to a shorter-acting agent and then stopping abruptly increases the severity and speed of withdrawal rather than easing it.

This child shows features of inattention and hyperactivity-impulsivity present across multiple settings (school, home and activities) for more than 6 months, consistent with ADHD. NICE guidance recommends that a formal ADHD diagnosis and initiation of pharmacological treatment should be made by a specialist service (paediatrics or CAMHS), not in primary care. The GP's role is to recognise the pattern of symptoms across settings and refer appropriately rather than initiating stimulant medication. Symptoms occurring in only one setting would be less suggestive of ADHD and might prompt consideration of other explanations.

• A. Dietary modification is not evidence-based as the sole management and should not substitute for specialist assessment and recognised treatment pathways.
• B. While educational input is valuable, a medical/psychiatric assessment is needed to formally evaluate for ADHD; this should not replace specialist referral.
• C. Methylphenidate should only be initiated by a specialist following formal diagnostic assessment, not by a GP.
• D. The behaviours described are pervasive across multiple settings and have persisted for over a year, which is not consistent with normal variation and warrants assessment.

This child demonstrates the core features of autism spectrum disorder: persistent deficits in social communication (reduced eye contact, lack of joint attention/pointing) and restricted, repetitive patterns of behaviour (insistence on routine, repetitive lining up of toys, lack of imaginative play). The preserved attention and lack of hyperactivity when engaged argue against ADHD, which is primarily characterised by inattention, hyperactivity and impulsivity rather than social communication deficits. Language delay can occur in autism but is a feature rather than the primary diagnosis, and the social and behavioural pattern described points to autism rather than an isolated language disorder.

• A. Social anxiety disorder involves fear of social situations rather than a fundamental lack of social communication skills and repetitive behaviours from early childhood.
• B. ADHD is characterised by inattention, hyperactivity and impulsivity; this child shows good attention and no fidgeting when engaged, and the core problem is social communication and repetitive behaviour.
• D. Oppositional defiant disorder involves a pattern of defiant, hostile behaviour towards authority figures, which is not described in this scenario.
• E. Specific language impairment involves delayed language without the accompanying social communication deficits and repetitive behaviours described here.

Conduct disorder is characterised by a repetitive, persistent pattern of behaviour that violates the basic rights of others or major age-appropriate societal norms, including aggression to people or animals, destruction of property, deceitfulness or theft, and serious rule violations. This case shows cruelty to animals, fire-setting, and theft, which are more severe violations than the defiant, non-compliant behaviour seen in oppositional defiant disorder. ODD involves angry, argumentative behaviour towards authority figures without the serious rights violations seen here. The diagnosis of conduct disorder is made under age 18; antisocial personality disorder cannot be diagnosed until age 18 and requires evidence of conduct disorder before age 15.

• A. There is no mention of inattention, hyperactivity or impulsivity typical of ADHD.
• C. Adjustment disorder follows an identifiable stressor with a shorter, less severe symptom pattern.
• D. ODD involves defiant, hostile behaviour towards authority figures but not serious violations such as cruelty to animals or fire-setting.
• E. This diagnosis cannot be made before age 18.

Delirium characteristically has an acute onset (hours to days) with a fluctuating course and impaired level of consciousness, whereas dementia has an insidious onset over months to years with a stable or slowly progressive course and preserved consciousness until late stages. Hallucinations and disorientation can occur in both conditions, so they do not reliably distinguish between them. The temporal course and conscious level are the key discriminating features used clinically. Her rapid onset over days, fluctuating clarity, and drowsiness are classic for delirium superimposed on an acute infection.

• A. Disorientation occurs in both delirium and dementia and does not distinguish between them.
• B. An infective trigger supports delirium but is not itself a clinical feature distinguishing the two conditions.
• C. Hallucinations can occur in both delirium and dementia, particularly Lewy body dementia, so this is not discriminating.
• E. Age alone does not differentiate delirium from dementia; both become more common with age.

The 4AT is a brief, validated bedside screening tool recommended by NICE for rapid assessment of delirium, assessing alertness, orientation (AMT4), attention (months backwards), and acute change or fluctuating course. It takes under 2 minutes, requires no special training, and does not require the patient's baseline cognitive state to be known in detail, making it ideal for acute ward settings. The MMSE and MoCA are longer tests designed to assess baseline cognitive impairment in dementia and are not validated for acute delirium screening, and are also unreliable in an acutely fluctuating patient. The GCS assesses conscious level after head injury or in critical illness, not delirium specifically.

• A. The MMSE is designed to assess cognitive impairment in a stable patient and is too lengthy and unreliable in acute delirium.
• B. The MoCA is used to screen for mild cognitive impairment and dementia, not for acute delirium.
• D. This tool screens for depression, not for an acute confusional state.
• E. The GCS assesses conscious level, typically in trauma or critical illness, and is not a delirium screening tool.

This patient's capillary blood glucose of 3.1 mmol/L confirms hypoglycaemia, a well-recognised and readily reversible cause of acute confusion, particularly in elderly patients on sulfonylureas such as gliclazide, which stimulate insulin release independent of food intake. Reversible causes of delirium are classically screened for using a systematic approach covering infection, metabolic derangement (including glucose, electrolytes, renal and hepatic function), and medications. While co-codamol could theoretically contribute to sedation, the biochemical confirmation of hypoglycaemia makes this the best-supported mechanism here. Correcting the blood glucose should be the immediate priority.

• B. Metformin does not cause hepatic encephalopathy; it is renally excreted and associated with lactic acidosis in overdose, not this picture.
• C. Hyperosmolar hyperglycaemic state occurs with very high, not low, blood glucose levels.
• D. While opioids can cause confusion, the confirmed hypoglycaemia is the more direct and biochemically supported explanation here.
• E. There are no fever, tachycardia or other signs suggesting infection in this patient.

NICE guidance recommends non-pharmacological measures as first-line management of delirium, including reorientation (clocks, calendars, consistent staff), ensuring adequate lighting, correcting sensory impairment, promoting normal sleep-wake cycles, and encouraging family involvement. Pharmacological treatment with antipsychotics such as haloperidol should be reserved for patients who are severely distressed or pose a risk to themselves or others despite these measures. This patient is agitated but not aggressive or at immediate risk, so environmental and behavioural strategies should be tried first. Physical restraint should be avoided wherever possible as it can worsen agitation and carries risks of injury.

• A. Benzodiazepines are not first-line for delirium and can worsen confusion except in alcohol withdrawal or seizures.
• C. This is excessive and not supported as an initial step before simple reorientation strategies are tried.
• D. Antipsychotics are reserved for patients who remain severely distressed or at risk despite non-drug measures; this is not yet first-line here.
• E. Restraint should be avoided as first-line management as it increases distress and injury risk.

Dementia with Lewy bodies is characterised by the core features of fluctuating cognition, recurrent visual hallucinations, spontaneous parkinsonism (bradykinesia, resting tremor, shuffling gait), and REM sleep behaviour disorder, all of which are present in this patient. Alzheimer's disease typically presents with gradual, progressive memory loss without early parkinsonism or prominent hallucinations. Vascular dementia classically shows a stepwise decline with focal neurological signs and vascular risk factors rather than fluctuating cognition and hallucinations. Frontotemporal dementia presents with early personality and behavioural change or language impairment, with memory relatively preserved early on.

• A. Vascular dementia typically shows stepwise decline with focal neurological deficits related to vascular events, not fluctuating cognition with hallucinations.
• C. Frontotemporal dementia presents with early behavioural or language changes, not parkinsonism and visual hallucinations.
• D. Alzheimer's disease presents with progressive memory impairment, not fluctuating cognition with early parkinsonism and hallucinations.
• E. Normal pressure hydrocephalus classically presents with the triad of gait disturbance, urinary incontinence and cognitive decline, without prominent hallucinations or REM sleep behaviour disorder.

Patients with dementia with Lewy bodies have a markedly increased sensitivity to antipsychotics, particularly typical agents like haloperidol, which can precipitate a severe neuroleptic sensitivity reaction characterised by acute worsening of parkinsonism, severe rigidity, autonomic instability, and impaired consciousness, sometimes with features resembling neuroleptic malignant syndrome. This occurs because Lewy body pathology already causes significant dopaminergic deficit, and dopamine blockade can produce an exaggerated extrapyramidal response. Antipsychotics should be avoided where possible in this group, and if essential, used only at the lowest possible dose with specialist advice, often favouring agents with lower dopamine affinity. This sensitivity reaction is a specific and well-recognised hazard distinct from the general risks of antipsychotic use in other dementias.

• A. Tardive dyskinesia is a risk with long-term antipsychotic use generally, but it is not the specific hazard highlighted in Lewy body dementia.
• B. Serotonin syndrome is associated with serotonergic drugs, not typically with haloperidol, and is not the specific concern in Lewy body dementia.
• C. QT prolongation is a recognised risk with antipsychotics in general but is not the specific sensitivity reaction associated with Lewy body dementia.
• E. There is no established evidence that antipsychotics accelerate the underlying neurodegenerative process itself.

Capacity assessment under the Mental Capacity Act 2005 requires evaluating whether the patient can understand, retain, use or weigh, and communicate information relevant to the decision. A patient may be able to repeat information back (understanding) yet still lack capacity if a delusional belief prevents them from weighing that information rationally to reach a decision, which is a distinct element of the capacity test. This patient's fixed delusion that the treatment is poison, despite correct factual recall, suggests his psychiatric illness may be impairing the weighing component of capacity, which must be specifically assessed before concluding he can validly refuse. Capacity is decision-specific and time-specific, so this must be formally evaluated rather than assumed from his ability to repeat information.

• B. The Mental Health Act governs treatment for mental disorder, not physical illness, and capacity must first be formally assessed; it is not an immediate step bypassing assessment.
• C. Next of kin cannot give or withhold consent for treatment decisions regarding another competent adult in England and Wales.
• D. A second opinion may be useful in complex cases but is not the immediate required step before assessing the weighing element of capacity.
• E. His ability to repeat information does not confirm he can weigh it, so his refusal cannot yet be accepted as valid without further assessment.

This woman has acute-onset psychotic symptoms (persecutory and delusional beliefs about her baby) in the postnatal period, which is a psychiatric emergency until proven otherwise. Puerperal (postpartum) psychosis typically presents within the first 2-4 weeks postpartum with rapid onset of mood disturbance, delusions, hallucinations or confusion, and carries significant risk to both mother and infant, including risk of harm to the baby or suicide. NICE guidance recommends urgent same-day assessment by specialist perinatal mental health services and admission, ideally to a mother and baby unit, so that the mother-infant bond can be preserved while she is treated and monitored. General psychiatric wards without mother and baby facilities and separation from the infant should be avoided unless specifically indicated for safety reasons.

• A. A routine outpatient referral underestimates the urgency; this requires same-day specialist assessment and likely admission.
• B. CBT and safety-netting are inappropriate for an acute psychotic presentation requiring urgent psychiatric assessment.
• C. Starting an antidepressant in primary care and reviewing in a week is unsafe given the acuity and risk of psychosis.
• E. Mother and baby units exist specifically to avoid unnecessary separation; a general ward should only be used if no mother and baby unit bed is available and risk assessment supports separation.