Q1. Which triad defines diabetic ketoacidosis? A. Hyperglycaemia, ketonaemia, metabolic acidosis B. Hyperglycaemia, hypernatraemia, alkalosis C. Hypoglycaemia, ketonaemia, acidosis D. Hyperglycaemia, raised osmolality, no ketones ANSWER: A. Why: all three must be present — glucose > 11 (or known diabetes), ketones ≥ 3 mmol/L, and pH < 7.3 or bicarbonate < 15. D: describes HHS, not DKA. LEARNING POINT: DKA is a three-part diagnosis, not simply a high glucose.

Q2. Why is serum potassium often normal or high at presentation in DKA despite total body depletion? A. The kidneys retain potassium in acidosis B. Acidosis and insulin deficiency shift K⁺ out of cells C. Ketones are potassium salts D. Dehydration destroys red cells ANSWER: B. Why: both acidosis and the absence of insulin move potassium from the intracellular to the extracellular compartment, raising the measured value while the body is being depleted through the urine. LEARNING POINT: the serum value reflects distribution, not total stores.

Q3. A patient in DKA has K⁺ 3.0 mmol/L. The correct immediate action is: A. Start the insulin infusion at once B. Give fluid and potassium; withhold insulin until K⁺ > 3.5 C. Give a large insulin bolus D. Give sodium bicarbonate ANSWER: B. Why: insulin drives potassium into cells. In a patient already hypokalaemic with profound total-body depletion, that can precipitate a fatal arrhythmia. D: bicarbonate is not routine in DKA and does not address the potassium. LEARNING POINT: potassium below 3.5 delays insulin. This is the single most important sequencing rule in the topic.

Q4. Six hours into DKA treatment: glucose 11 mmol/L, ketones 3.6, pH 7.21. The correct action is: A. Stop the insulin infusion B. Continue insulin and start intravenous dextrose C. Halve the fluid rate D. Give subcutaneous insulin and stop the infusion ANSWER: B — continue insulin, add dextrose. Why: insulin is being given to switch off ketogenesis, and the ketones and acidosis have not resolved. Dextrose supports the glucose so the infusion can continue safely. A, D: stopping early allows the ketoacidosis to persist. LEARNING POINT: the endpoint is ketone clearance, not a normal glucose.

Q5. An 82-year-old with type 2 diabetes, unwell for four days: glucose 44, ketones 0.4, pH 7.38, osmolality 355. The diagnosis and key management principle are: A. DKA; rapid insulin infusion B. HHS; cautious fluid replacement and thromboprophylaxis C. DKA; immediate bicarbonate D. Simple hyperglycaemia; oral agents ANSWER: B — HHS. Why: very high glucose with minimal ketones, no acidosis and markedly raised osmolality over several days is the hyperosmolar state. Correction must be gradual, and thrombosis risk is high. A, C: there is no ketoacidosis. D: this patient is critically unwell. LEARNING POINT: HHS carries HIGHER mortality than DKA despite looking less dramatic.

Q6. A 10-year-old being treated for DKA improves biochemically but becomes drowsy with a headache six hours in. The most concerning diagnosis is: A. Hypoglycaemia B. Cerebral oedema C. Hyperkalaemia D. Resolution of the DKA ANSWER: B — cerebral oedema. Why: it is a rare but frequently fatal complication, mainly in children and young people, associated with rapid osmolar shifts during treatment. Neurological deterioration WHILE the biochemistry improves is the classic pattern. A: possible, but readily excluded by a glucose check. D: improvement does not cause drowsiness. LEARNING POINT: a patient getting sleepier as their gas improves is a red flag, not reassurance.

Q7. A patient on empagliflozin has vomiting, abdominal pain, pH 7.18, ketones 4.2, glucose 9.4 mmol/L. The diagnosis is: A. DKA is excluded by the glucose B. Euglycaemic DKA C. Lactic acidosis from metformin D. Hyperosmolar state ANSWER: B — euglycaemic DKA. Why: SGLT2 inhibitors excrete glucose renally, so genuine ketoacidosis can occur with a normal or near-normal glucose. The ketones and acidosis make the diagnosis. A: the trap — screening by glucose alone misses this. D: HHS has minimal ketones and no acidosis. LEARNING POINT: on an SGLT2 inhibitor, the glucose cannot be used to exclude DKA.