Ten single-best-answer clinical vignettes covering type 1 and type 2 diabetes, acute emergencies (DKA, HHS, hypoglycaemia), chronic complications, pharmacology and interpretation of basic investigations. Answer key (concise reasoning): Q1: B — Typical presentation (young, weight loss, ketonuria, positive autoantibodies) fits type 1 diabetes. Q2: D — In DKA with serum K >5.5 mmol/L, do not give potassium replacement; start IV insulin after initial fluid resuscitation and monitor K. Q3: A — Severe neuroglycopaenia with IV access requires IV 50% dextrose bolus (faster and more reliable than oral/IM if IV available). Q4: E — SGLT2 inhibitors cause renal glucose loss (glycosuria), lowering plasma glucose while permitting ketogenesis (euglycaemic DKA). Q5: C — HbA1c 8.2% corresponds to an estimated average glucose ≈10.5 mmol/L (use eAG conversion: ~28.7×A1c−46.7 mg/dL). Q6: A — New microalbuminuria in type 2 diabetes should prompt an ACE inhibitor (or ARB) to reduce progression, even if BP is only mildly elevated. Q7: D — ABPI ≈0.6 indicates moderate peripheral arterial disease; urgent vascular assessment for possible revascularisation is needed for a non-healing diabetic foot ulcer. Q8: B — Basal–bolus multiple daily injections (or pump therapy) gives best control of fasting and post-prandial glucose in type 1 diabetes. Q9: E — If serum K <3.3 mmol/L in DKA, potassium must be replaced before starting insulin to avoid life-threatening hypokalaemia. Q10: C — Urine dipsticks detect acetoacetate; in DKA beta‑hydroxybutyrate predominates, so blood BHB measurement is more accurate.
USMAN GHANI AWAN @usmanawan
Medical Student
