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EMREE psychiatry practice questions

Original EMREE questions on psychiatry, with explanations.

Short answer: 10 original multiple-choice practice questions on psychiatry for EMREE, the Emirates Medical Residency Entrance Examination, each with the correct answer and a full explanation. The blueprint gives this subject 10 percent of the exam. They are original and are not real exam items.

About these questions
  • Every question here is original. Meddex wrote it for exam preparation. None is a real, recalled or leaked exam item, and none comes from DHA, Prometric, UAE University or the NIHS.
  • Meddex is independent and is not affiliated with DHA, Prometric, UAE University or the NIHS.
  • Clinical review of the question bank is not complete yet. Treat the explanations as study aids and check official guidance before you rely on a fact.
  • This is a sample, not the whole bank, and doing well on it does not predict an exam result.

What psychiatry covers

Mood, psychotic, anxiety and substance disorders, psychiatric emergencies and psychopharmacology.

Assess risk first, then diagnose, then choose the treatment and the setting. Many items test safe prescribing and capacity.

Where it fits in the exam

The organiser's EMREE blueprint (November 2025 edition) gives Psychiatry 10 percent of the exam, which is about 12 of 120 questions. It says the distribution may differ by up to 5 percent in each category. These weights are official, and the question counts are our arithmetic.

The organiser does not state how many answer options its questions have or whether each has one best answer. Meddex practice items use four options with one best answer, as a practice format.

How to use these questions

Decide your answer before you press Show answer. Then read the reason for every option, including the ones you rejected. Note the idea you missed and come back to it in a few days.

Practice questions

  1. Question 1

    PsychiatryMedium

    A 44-year-old man with schizophrenia is taking haloperidol 10 mg daily. A routine ECG shows a QTc of 515 ms, compared with 430 ms at baseline. He is asymptomatic, and potassium and magnesium are normal. He takes no other medication. What is the most appropriate management?

    • Option A: Continue unchanged and repeat the ECG in a year
    • Option B: Switch to a low-QT antipsychotic such as aripiprazole and repeat the ECG
    • Option C: Add propranolol to shorten the QT interval
    • Option D: Add magnesium and potassium and continue haloperidol unchanged
    Show answer for question 1

    Correct answer: B. Switch to a low-QT antipsychotic such as aripiprazole and repeat the ECG

    A QTc above 500 ms, or a rise of more than 60 ms from baseline, raises the risk of torsades de pointes and sudden death. The management is to remove or switch the culprit, correct electrolytes and avoid other QT-prolonging drugs, with repeat ECG. Aripiprazole has little effect on QTc. Beta-blockers do not shorten the QT interval in drug-induced prolongation.

    • Why A is wrong. Continuing with a markedly prolonged QTc exposes him to avoidable arrhythmia risk.
    • Why C is wrong. Propranolol does not correct drug-induced QT prolongation.
    • Why D is wrong. Magnesium is only useful for deficiency or active torsades and does not remove the underlying risk.

    Topic: Schizophrenia: antipsychotic QT prolongation. Reference: 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death (Priori et al.); Maudsley Prescribing Guidelines in Psychiatry; APA Practice Guideline for the Treatment of Patients with Schizophrenia (2020)

  2. Question 2

    PsychiatryMedium

    A 40-year-old man with bipolar disorder has taken lithium for 12 years with a level of 0.7 mmol/L. He now has polyuria of 5 litres a day and marked thirst. Serum sodium is 146 mmol/L and corrected calcium is normal. After water deprivation his urine osmolality stays at 180 mOsm/kg with no rise after desmopressin. What is the most likely diagnosis?

    • Option A: Nephrogenic diabetes insipidus due to lithium
    • Option B: Central diabetes insipidus
    • Option C: Primary polydipsia
    • Option D: Hypercalcaemia from lithium-associated hyperparathyroidism
    Show answer for question 2

    Correct answer: A. Nephrogenic diabetes insipidus due to lithium

    Lithium impairs the response of the collecting duct to vasopressin and is the commonest cause of drug-induced nephrogenic diabetes insipidus. The failure to concentrate urine after both water deprivation and desmopressin points to a renal rather than pituitary cause. Management includes assessing renal function, amiloride, and considering a change of mood stabiliser if severe or if renal function is declining.

    • Why B is wrong. Central diabetes insipidus would concentrate urine after desmopressin.
    • Why C is wrong. Primary polydipsia would concentrate urine with water deprivation and cause low sodium.
    • Why D is wrong. Calcium is normal, so hypercalcaemia does not explain the polyuria.

    Topic: Lithium: nephrogenic diabetes insipidus. Reference: NICE CG185 Bipolar disorder: assessment and management; British Association for Psychopharmacology guidelines for bipolar disorder (Goodwin et al. 2016); Maudsley Prescribing Guidelines in Psychiatry

  3. Question 3

    PsychiatryEasy

    A 35-year-old woman ran out of paroxetine 40 mg and stopped it abruptly 3 days ago. She now has dizziness, electric-shock sensations, nausea, irritability and insomnia. She is afebrile with normal tone and reflexes and has no suicidal thoughts. What is the most appropriate management?

    • Option A: Start an antipsychotic
    • Option B: Admit to exclude serotonin syndrome
    • Option C: Start regular lorazepam for two weeks to cover the symptoms
    • Option D: Restart paroxetine and taper more slowly
    Show answer for question 3

    Correct answer: D. Restart paroxetine and taper more slowly

    Abrupt cessation of a short half-life antidepressant such as paroxetine commonly causes discontinuation symptoms within days, including sensory disturbance, dizziness, nausea and insomnia. Absent fever, hyperreflexia or clonus, serotonin syndrome is unlikely. Restarting the drug and tapering gradually (or switching to a longer-acting agent) relieves symptoms.

    • Why A is wrong. Antipsychotics have no role and carry their own adverse effects.
    • Why B is wrong. Normal tone, reflexes and temperature make serotonin syndrome unlikely and admission unnecessary.
    • Why C is wrong. Benzodiazepines do not address the cause and add dependence risk.

    Topic: Antidepressant discontinuation syndrome. Reference: NICE NG215 Medicines associated with dependence or withdrawal symptoms; NICE NG222 Depression in adults; Maudsley Prescribing Guidelines in Psychiatry

  4. Question 4

    PsychiatryMedium

    A 27-year-old woman with stable schizophrenia on risperidone 4 mg daily has had 6 months of oligomenorrhoea progressing to amenorrhoea, with galactorrhoea. Pregnancy test is negative, prolactin is 3100 mIU/L (reference under 500) and TSH is normal. She has no headache or visual symptoms. What is the most appropriate next step?

    • Option A: Refer urgently for pituitary surgery
    • Option B: Start cabergoline
    • Option C: Add oestrogen replacement for the amenorrhoea and continue risperidone unchanged
    • Option D: Switch risperidone to a prolactin-sparing antipsychotic such as aripiprazole
    Show answer for question 4

    Correct answer: D. Switch risperidone to a prolactin-sparing antipsychotic such as aripiprazole

    Risperidone is a potent cause of hyperprolactinaemia through D2 blockade in the pituitary, producing amenorrhoea, galactorrhoea and long-term bone loss. After excluding pregnancy and hypothyroidism, the usual step is to change to a prolactin-sparing agent such as aripiprazole, with pituitary imaging if the level does not normalise or symptoms of a mass emerge. Dopamine agonists can worsen psychosis.

    • Why A is wrong. Surgery is unwarranted in a drug-induced elevation without mass symptoms.
    • Why B is wrong. Cabergoline is a dopamine agonist that may precipitate psychotic relapse.
    • Why C is wrong. Oestrogen treats the consequence but leaves the cause and galactorrhoea in place.

    Topic: Schizophrenia: antipsychotic-induced hyperprolactinaemia. Reference: Endocrine Society Clinical Practice Guideline: Diagnosis and treatment of hyperprolactinemia (2011); Maudsley Prescribing Guidelines in Psychiatry; NICE CG178 Psychosis and schizophrenia in adults

  5. Question 5

    PsychiatryMedium

    A 45-year-old man has had a major depressive episode for 7 months. Adherence is confirmed for sertraline 150 mg for 10 weeks and then venlafaxine 225 mg for 10 weeks, with no meaningful response. He has no psychotic features. What is the most appropriate next step?

    • Option A: Add nightly zopiclone and review in two weeks
    • Option B: Augment with a second-generation antipsychotic such as aripiprazole, alongside psychological therapy
    • Option C: Add St John's wort to venlafaxine
    • Option D: Continue venlafaxine unchanged for 12 more weeks
    Show answer for question 5

    Correct answer: B. Augment with a second-generation antipsychotic such as aripiprazole, alongside psychological therapy

    After two adequate antidepressant trials, treatment-resistant depression is managed by augmentation (an atypical antipsychotic such as aripiprazole or quetiapine, or lithium) or by combination or switching, with structured psychological therapy and consideration of ECT if severe. St John's wort with a serotonergic drug risks serotonin syndrome.

    • Why A is wrong. Hypnotics treat sleep only and do not treat depression.
    • Why C is wrong. The herb has variable potency and interacts dangerously with serotonergic antidepressants.
    • Why D is wrong. Further waiting on an adequate failed trial offers little chance of benefit.

    Topic: Depression: treatment-resistant episode. Reference: NICE NG222 Depression in adults; CANMAT 2016 Clinical guidelines for the management of adults with major depressive disorder: Pharmacological treatments; APA Practice Guideline for the Treatment of Patients with Major Depressive Disorder

  6. Question 6

    PsychiatryEasy

    A 26-year-old woman has recurrent unexpected attacks of palpitations, chest tightness and fear of dying, and now avoids travelling by train. ECG and TSH are normal, and she uses no substances. Which is the most appropriate initial treatment?

    • Option A: Cognitive behavioural therapy, with an SSRI if she prefers medication
    • Option B: Buspirone as monotherapy
    • Option C: Propranolol as monotherapy
    • Option D: Regular alprazolam, with an SSRI added only if the attacks persist after three months
    Show answer for question 6

    Correct answer: A. Cognitive behavioural therapy, with an SSRI if she prefers medication

    Panic disorder is treated with CBT or an SSRI (or both). Benzodiazepines give quick relief but carry dependence risk and no lasting benefit, and should be avoided long term. Beta-blockers and buspirone lack evidence in panic disorder. SSRIs are started at low doses because early anxiety can worsen transiently.

    • Why B is wrong. Buspirone has not been shown to be effective for panic disorder.
    • Why C is wrong. Beta-blockers do not prevent panic attacks.
    • Why D is wrong. Benzodiazepines risk dependence and are not recommended for ongoing panic disorder.

    Topic: Anxiety: panic disorder treatment. Reference: NICE CG113 Generalised anxiety disorder and panic disorder in adults; APA Practice Guideline for the Treatment of Patients with Panic Disorder; WFSBP Guidelines for the pharmacological treatment of anxiety, OCD and PTSD

  7. Question 7

    PsychiatryMedium

    The mother of a 16-year-old boy asks whether he has antisocial personality disorder. Since age 11 he has bullied others, set fires, stolen repeatedly and shown little remorse. Which statement is most accurate?

    • Option A: He meets criteria for conduct disorder; the diagnosis needs age 18 or older
    • Option B: He can be diagnosed now because the pattern has lasted more than five years
    • Option C: The diagnosis requires at least one proven criminal conviction in adulthood
    • Option D: The diagnosis excludes any history of conduct disorder in childhood or adolescence
    Show answer for question 7

    Correct answer: A. He meets criteria for conduct disorder; the diagnosis needs age 18 or older

    Antisocial personality disorder is a diagnosis made from the age of 18, and it requires evidence of conduct disorder with onset before age 15. In this adolescent the pattern fits conduct disorder, which can be specified with limited prosocial emotions. Convictions are not required for the diagnosis, and a childhood history of conduct disorder is a prerequisite rather than an exclusion.

    • Why B is wrong. The duration of the behaviour does not remove the age requirement.
    • Why C is wrong. Criminal convictions are not required to diagnose the disorder.
    • Why D is wrong. Conduct disorder before age 15 is part of the criteria rather than an exclusion.

    Topic: Personality disorder: antisocial personality disorder diagnosis. Reference: DSM-5-TR Diagnostic and Statistical Manual of Mental Disorders (antisocial personality disorder; conduct disorder)

  8. Question 8

    PsychiatryMedium

    A 23-year-old man who has used ketamine most days for 2 years has 4 months of urinary frequency, urgency, suprapubic pain and episodes of visible haematuria. Urine cultures are repeatedly sterile and ultrasound shows a thick-walled, small-capacity bladder. Which is the most appropriate core management?

    • Option A: Repeated courses of antibiotics for presumed recurrent bacterial cystitis
    • Option B: Support to stop ketamine, with urology referral and symptom relief
    • Option C: Early augmentation cystoplasty to restore his bladder capacity
    • Option D: An antimuscarinic drug alone, advising that ketamine can be continued
    Show answer for question 8

    Correct answer: B. Support to stop ketamine, with urology referral and symptom relief

    Chronic ketamine use causes a toxic cystitis, with sterile pyuria or haematuria, a small contracted bladder and sometimes upper tract obstruction. Stopping ketamine is the mainstay of treatment and often improves symptoms, while relapse of urinary symptoms is usual if use resumes. Analgesia, antimuscarinics and intravesical treatments are supportive, imaging looks for hydronephrosis, and surgery is a last resort for severe, refractory disease.

    • Why A is wrong. Cultures are sterile, so antibiotics do not treat the cause and add avoidable adverse effects.
    • Why C is wrong. Reconstructive surgery is a last resort once cessation and conservative treatment have failed.
    • Why D is wrong. Symptomatic drugs are of limited benefit while exposure to the bladder toxin continues.

    Topic: Substance use: ketamine-associated bladder damage. Reference: Management of ketamine cystitis: national guidelines from the French Association of Urology (CUROPF/CTMH), 2024

  9. Question 9

    PsychiatryEasy

    A 27-year-old man has had repeated 3-day episodes of intense vomiting over 18 months. He finds that long hot showers relieve the nausea. He has smoked cannabis daily for 8 years. Bloods, abdominal imaging and endoscopy are normal. Which is the most appropriate advice?

    • Option A: Refer for surgical opinion on gastric emptying procedures
    • Option B: Advise sustained cannabis cessation, with topical capsaicin for acute episodes
    • Option C: Start a proton pump inhibitor and let him continue cannabis in smaller amounts
    • Option D: Prescribe regular opioid analgesia for the recurrent abdominal pain and vomiting
    Show answer for question 9

    Correct answer: B. Advise sustained cannabis cessation, with topical capsaicin for acute episodes

    Cannabis hyperemesis syndrome occurs in long-term heavy users and causes cyclical vomiting relieved by hot bathing. The only definitive treatment is sustained cessation of cannabis. Topical capsaicin and antiemetics such as haloperidol can reduce symptoms in acute episodes, and standard antiemetics are often ineffective. Opioids worsen nausea, and reducing rather than stopping use does not reliably prevent recurrence.

    • Why A is wrong. Surgery has no role when imaging and endoscopy are normal.
    • Why C is wrong. Proton pump inhibitors do not treat this condition, and continued use perpetuates it.
    • Why D is wrong. Opioids cause nausea and vomiting and add dependence risk.

    Topic: Substance use: cannabis hyperemesis syndrome. Reference: Sorensen CJ et al. Cannabinoid hyperemesis syndrome: diagnosis, pathophysiology, and treatment: a systematic review. J Med Toxicol 2017

  10. Question 10

    PsychiatryMedium

    A 49-year-old man who drinks heavily every day is admitted with a chest infection. He is thin and has a poor diet. He is alert and oriented, walks steadily and has normal eye movements, and his capillary glucose is 5.2 mmol/L. Which is the most appropriate plan for thiamine?

    • Option A: Oral folic acid 5 mg daily, since folate is the usual deficiency
    • Option B: Intravenous glucose first, with vitamins to follow later
    • Option C: None, because he has no confusion, ataxia or eye signs
    • Option D: Prophylactic parenteral thiamine, followed by oral thiamine
    Show answer for question 10

    Correct answer: D. Prophylactic parenteral thiamine, followed by oral thiamine

    Harmful or dependent drinkers who are malnourished and admitted with an acute illness are at high risk of Wernicke encephalopathy, and the classic triad is often absent. NICE advises prophylactic parenteral thiamine followed by oral thiamine for these patients. Waiting for signs risks irreversible Korsakoff syndrome, and carbohydrate given without thiamine can precipitate the encephalopathy. Folic acid does not replace thiamine, and treatment doses are higher once symptoms of Wernicke encephalopathy appear.

    • Why A is wrong. Folic acid treats folate deficiency and does not replace thiamine.
    • Why B is wrong. Glucose without thiamine can precipitate Wernicke encephalopathy.
    • Why C is wrong. Wernicke encephalopathy is often present without the full triad, so waiting for signs risks permanent brain damage.

    Topic: Alcohol: thiamine in a malnourished heavy drinker. Reference: NICE CG100 Alcohol-use disorders: diagnosis and management of physical complications

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