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DOH · DHA · MOH — General Practitioner

DOH, DHA & MOH GP (General Practitioner) Exam Questions

Practice questions for the UAE GP licensing exams (DOH, DHA and MOH Prometric), each with a worked explanation, the wrong-option traps, and the guideline it rests on. Built by an MRCP-qualified doctor.

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Q1 Diabetes Management

A 52-year-old man with type 2 diabetes and established ischaemic heart disease presents for a medication review. His HbA1c is 72 mmol/mol (8.7%) despite being on metformin 1 g twice daily for the past 12 months. He has no heart failure and his eGFR is 68 mL/min/1.73 m². What is the most appropriate add-on therapy?

  • A Sulphonylurea (e.g., gliclazide)
  • B SGLT-2 inhibitor (e.g., empagliflozin)
  • C Basal insulin (e.g., insulin glargine)
  • D DPP-4 inhibitor (e.g., sitagliptin)
Model answer + full explanation

In type 2 diabetes with established atherosclerotic cardiovascular disease (ASCVD) and suboptimal glycaemic control on metformin, an SGLT-2 inhibitor is the preferred add-on agent regardless of HbA1c target, per ADA 2025 Standards of Care (Section 9) and NICE NG28. Empagliflozin (EMPA-REG OUTCOME) and dapagliflozin (DECLARE-TIMI 58) both demonstrated significant reductions in MACE, cardiovascular mortality, and HF hospitalisation. Adding eGFR context (68 mL/min/1.73 m²) confirms SGLT-2 inhibitor eligibility. Sulphonylureas reduce HbA1c but carry hypoglycaemia risk and confer no CV benefit. DPP-4 inhibitors are weight-neutral and safe but lack proven CV outcome benefit beyond non-inferiority. Basal insulin is appropriate for more refractory hyperglycaemia or symptomatic cases, not as a second-line agent in stable ASCVD. Clinical pearl: in T2DM with ASCVD, CV risk reduction — not just glucose lowering — should drive agent selection.

Q2 Hyperthyroidism

A 52-year-old woman presents to her GP with a 3-month history of palpitations, heat intolerance, and a 4 kg unintentional weight loss. On examination she has a painless, diffuse, firm neck swelling with a mild tremor of the outstretched hands. TFTs show a suppressed TSH (<0.01 mU/L) and an elevated free T4. What is the most likely diagnosis?

  • A Hashimoto's thyroiditis
  • B Toxic multinodular goitre
  • C Graves' disease
  • D De Quervain's thyroiditis
  • E Thyroid cancer
Model answer + full explanation

Graves' disease is the most likely diagnosis. It is the commonest cause of hyperthyroidism in women of working age and is caused by TSH-receptor stimulating antibodies (TRAb), producing a diffuse goitre with biochemical thyrotoxicosis (suppressed TSH, elevated free T4/T3). Associated symptoms — palpitations, weight loss, heat intolerance, and tremor — are classic. Per NICE NG145 (2023) and the ATA 2016 Hyperthyroidism Guidelines, TRAb measurement confirms the diagnosis and guides management. Toxic multinodular goitre (Plummer's disease) is an important alternative in older patients but typically produces a nodular rather than diffuse gland. Hashimoto's thyroiditis classically causes hypothyroidism; early hashitoxicosis is transient and TSH-receptor antibodies are absent. De Quervain's thyroiditis presents with a painful tender goitre following viral illness. Thyroid cancer typically presents as a firm solitary nodule, not diffuse enlargement, and does not cause biochemical thyrotoxicosis. Clinical pearl: bilateral exophthalmos, if present, is pathognomonic of Graves' disease and is not seen in any other cause of thyrotoxicosis.

Q3 Confidentiality

Ahmed, a 42-year-old Emirati taxi driver, attends your GP clinic for a routine follow-up. He was diagnosed with type 1 diabetes mellitus 18 months ago and has been on a basal-bolus insulin regimen. During today's consultation, he reports two episodes of hypoglycaemia in the past month that caused him to lose consciousness, one while at home and another while waiting at a taxi rank. His HbA1c is 58 mmol/mol (7.5%). He has no hypoglycaemic awareness symptoms preceding these episodes. He underwent laser photocoagulation for proliferative diabetic retinopathy six months ago, and his corrected visual acuity is 6/12 bilaterally. You counsel Ahmed that his recurrent hypoglycaemia with impaired awareness poses a significant risk while driving professionally and advise him to inform the relevant licensing authority. He becomes distressed and states he is the sole earner for his family of six and explicitly refuses to notify the licensing authority or stop driving. You document the discussion and send a follow-up letter reinforcing your advice. At a review appointment two weeks later, Ahmed confirms he has not informed the licensing authority and continues to drive his taxi daily. What is the most appropriate next step in managing this situation?

  • A Arrange urgent referral to an endocrinologist before taking any further action regarding driving
  • B Continue to counsel the patient and respect his autonomy regarding disclosure
  • C Discharge the patient from your practice for non-compliance with medical advice
  • D Disclose his medical condition to the licensing authority after informing the patient
  • E Prescribe a continuous glucose monitor and permit him to continue driving
Model answer + full explanation

Why correct (D): Confidentiality is a qualified duty, not absolute. When a patient with a medical condition that renders them unfit to drive refuses to inform the licensing authority despite repeated counselling, the physician has a justified duty to breach confidentiality in the interest of public safety. The General Medical Council (GMC) guidance 'Confidentiality: good practice in handling patient information' (2017, updated 2023) and analogous DVLA/licensing frameworks used in UAE practice state that if a patient continues to drive against medical advice and poses a serious risk to others, the doctor should (1) make every reasonable effort to persuade the patient to stop driving, (2) document the advice given, (3) inform the patient that disclosure will be made, and (4) then disclose the relevant medical information to the licensing authority. Ahmed has had two episodes of loss of consciousness from hypoglycaemia, including impaired hypoglycaemic awareness, and holds a Group 2 equivalent professional driving licence. He was counselled, given written advice, and at review still refuses to comply. The physician has exhausted reasonable persuasion and must now disclose to protect public safety, having informed the patient first.

Why A wrong: While endocrinology referral is clinically appropriate for optimising glycaemic control and managing hypoglycaemic unawareness, it does not address the immediate road safety risk. Referral should not delay the mandatory step of disclosure to the licensing authority when the patient continues to drive professionally despite recurrent loss of consciousness.

Why B wrong: Respecting patient autonomy is fundamental, but confidentiality is qualified, not absolute. When continued counselling has failed and there is a clear, serious risk of harm to the public (a professional driver with recurrent loss of consciousness), ongoing passive counselling alone is insufficient and would represent a failure of the physician's duty to protect third parties.

Why C wrong: Discharging a patient from the practice is not an appropriate response to this situation. It does not resolve the public safety risk, removes the therapeutic relationship needed for ongoing management, and is punitive rather than protective. The physician retains a duty to act on the known risk regardless of the patient's registration status.

Why E wrong: While continuous glucose monitoring (CGM) can improve hypoglycaemic awareness over time, it does not immediately resolve the unsafe driving situation. Prescribing a CGM and permitting continued professional driving in the presence of ongoing hypoglycaemic unawareness with loss of consciousness episodes would be clinically negligent, as the risk to public safety remains unacceptable in the interim.

Key learning point: Confidentiality is a qualified duty; when a patient with a condition rendering them medically unfit to drive refuses to stop driving or notify the licensing authority despite documented repeated counselling, the physician is ethically and legally justified in disclosing relevant medical information to the licensing authority to protect public safety, provided the patient is informed beforehand.

Q4 Febrile Convulsions

A 2-year-old with first febrile convulsion is alert and well post-ictal. Temperature is 38.8°C from URTI. Neurological examination normal. Is lumbar puncture indicated?

  • A Yes, always rule out meningitis
  • B No, if meningitis clinically excluded and no features of complex FC
  • C Yes, all children <18 months require LP
  • D Only if seizure complex (focal, prolonged, recurrent)
  • E Only if fever source unknown
Model answer + full explanation

Lumbar puncture not routinely indicated in simple FC if: (1) meningitis clinically excluded (no meningeal signs), (2) age >18 months, (3) seizure simple (generalised, <15 min, single). Consider LP if: complex FC, age <18 months, suspected meningitis, immunocompromised. NICE CG25.

Q5 Lithium Monitoring

A 47-year-old woman with bipolar affective disorder on lithium carbonate 800 mg twice daily presents to her GP with a 5-day history of coarse tremor, increasing confusion, nausea, and diarrhoea. She recently started a new medication for a urinary tract infection 8 days ago. Her blood pressure is 108/70 mmHg and she appears clinically dehydrated. Her lithium level (taken 12 hours after last dose) is 2.4 mmol/L (therapeutic range 0.6–1.0 mmol/L for maintenance). Which antibiotic most likely precipitated this, and what is the most appropriate immediate management?

  • A Trimethoprim — hold lithium, IV fluid resuscitation, and urgent nephrology review; haemodialysis may be required
  • B Nitrofurantoin — reduce lithium dose by half and reassure that levels will normalise with hydration
  • C Amoxicillin — continue lithium at same dose and treat symptoms; recheck levels in 1 week
  • D Cefalexin — stop lithium permanently and switch to valproate as the mood stabiliser
  • E Ciprofloxacin — stop lithium, give activated charcoal, and discharge with oral fluids
Model answer + full explanation

Trimethoprim reduces renal tubular secretion of lithium, significantly raising serum lithium levels — a well-recognised and dangerous drug interaction. Other nephrotoxins/diuretics (NSAIDs, thiazides, ACEi) similarly raise lithium levels. This patient has severe lithium toxicity (level 2.4 mmol/L, >2.0 = severe toxicity): coarse tremor, confusion, GI symptoms, and cardiovascular instability. Management of severe lithium toxicity: (1) Stop lithium immediately; (2) IV 0.9% NaCl to restore renal perfusion and enhance lithium excretion; (3) Urgent nephrology review — haemodialysis is indicated for levels >2.5 mmol/L or severe neurotoxicity (seizures, reduced consciousness) regardless of level; (4) Cardiac monitoring for arrhythmias. Activated charcoal does not bind lithium. Simply dose-reducing is insufficient for toxicity at this level.

Reference: NICE ENT Guidelines.

Topics covered in this bank

  • Diabetes Management
  • Hyperthyroidism
  • Confidentiality
  • Febrile Convulsions
  • Lithium Monitoring

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Frequently asked questions

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