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DKA, HHS & hypoglycaemia flashcards

22 high-yield MRCP Part 1 cards from the Intellect Medicos Endocrinology & Diabetes course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. What are the JBDS diagnostic criteria for diabetic ketoacidosis?

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    Ketones ≥3 mmol/L (or urine ≥2+); glucose >11 mmol/L or known diabetes; pH <7.3 and/or bicarbonate <15 mmol/L.

    Why? All three parts — ketonaemia, hyperglycaemia/diabetes and acidosis — are needed.

  2. What IV fluid is given in the first hour of DKA management in a normotensive adult?

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    0.9% sodium chloride, 1 litre over 1 hour.

    Why? Restoring circulating volume is the first priority. Later bags run over 2, 2, 4, 4 and 6 hours.

  3. What insulin infusion is used in DKA, and at what rate?

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    Fixed-rate IV infusion of soluble human insulin at 0.1 units/kg/hour.

    Why? A fixed rate clears ketones regardless of glucose. Estimate weight if needed.

  4. What should happen to a patient's usual long-acting insulin during DKA treatment?

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    Continue it at the usual dose and time.

    Why? This prevents rebound ketosis when the IV insulin is stopped.

  5. In DKA, how much potassium is added to each litre of fluid if serum K⁺ is 3.5–5.5 mmol/L?

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    40 mmol KCl per litre.

    Why? Insulin drives potassium into cells, so levels fall during treatment. Give no KCl if K⁺ >5.5; seek senior advice if <3.5.

  6. In DKA, when is 10% glucose added, and at what rate?

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    When blood glucose falls below 14 mmol/L — 10% glucose at 125 mL/hour alongside the saline.

    Why? This lets the fixed-rate insulin keep clearing ketones without causing hypoglycaemia. JBDS (2023) also suggests considering reducing the insulin to 0.05 units/kg/hour at this point.

  7. What hourly fall in blood ketones is the target in DKA, and what is done if it is not reached?

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    Fall of ≥0.5 mmol/L/hour; if not, increase the insulin infusion by 1 unit/hour.

    Why? Alternative targets: bicarbonate rising ≥3 mmol/L/hour or glucose falling ≥3 mmol/L/hour.

  8. What criteria define resolution of DKA?

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    Blood ketones <0.6 mmol/L and venous pH >7.3.

    Why? Bicarbonate is not used to judge resolution. Switch to subcutaneous insulin once DKA has resolved and the patient is eating and clinically stable.

  9. What are the key biochemical features of hyperosmolar hyperglycaemic state (HHS)?

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    Glucose >30 mmol/L, serum osmolality >320 mOsm/kg and no significant ketonaemia or acidosis.

    Why? Residual insulin suppresses ketogenesis but cannot control the glucose. It typically affects older people with type 2 diabetes.

  10. How is serum osmolality calculated in HHS?

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    2 × Na⁺ + glucose + urea (all in mmol/L).

    Why? Serial calculated osmolality guides the rate of correction.

  11. What is the first-line treatment of HHS?

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    IV 0.9% sodium chloride alone (even if hypernatraemic).

    Why? Fluids alone lower glucose and osmolality. Use 0.45% saline only if osmolality is not falling despite adequate fluid. Give prophylactic LMWH because of high VTE risk.

  12. In HHS, when is IV insulin started, and at what rate?

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    Only when glucose stops falling with fluids alone (or if significant ketonaemia), at 0.05 units/kg/hour.

    Why? Early insulin drops glucose and osmolality too fast, shifting water into cells and risking cerebral oedema and circulatory collapse.

  13. In HHS, what is the target rate of fall of serum osmolality?

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    3–8 mOsm/kg per hour.

    Why? Glucose should fall by no more than 5 mmol/L/hour and sodium by no more than 10 mmol/L in 24 hours.

  14. How is hypoglycaemia (<4 mmol/L) treated in a conscious adult who can swallow?

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    Fast-acting oral carbohydrate; recheck after about 15 minutes and repeat up to 3 times.

    Why? Follow with a longer-acting carbohydrate once glucose recovers. If still not responding, give IM glucagon or IV 10% glucose.

  15. For an unconscious hypoglycaemic patient, why should 50% glucose be avoided?

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    Risk of extravasation injury (it is highly irritant).

    Why? Use IM glucagon, or IV 10% or 20% glucose instead.

  16. In which situations is IM glucagon ineffective for hypoglycaemia?

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    When liver glycogen is depleted — prolonged fasting, chronic hypoglycaemia or alcohol-induced hypoglycaemia.

    Why? Glucagon works by releasing glucose from hepatic glycogen; with no glycogen, give IV glucose.

  17. What is the FIRST physiological defence against falling blood glucose?

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    Reduced insulin secretion.

    Why? Then glucagon rises, then adrenaline; growth hormone and cortisol respond later.

  18. How does alcohol cause hypoglycaemia?

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    Alcohol metabolism raises NADH, which inhibits hepatic gluconeogenesis.

    Why? Risk is highest after fasting or binge drinking, when glycogen stores are already low.

  19. What is Whipple's triad?

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    Symptoms of hypoglycaemia, a documented low plasma glucose, and relief of symptoms when glucose is given.

    Why? It must be shown before investigating for an insulinoma, the commonest pancreatic islet-cell tumour (about 90% benign).

  20. What is the gold-standard diagnostic test for insulinoma?

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    Supervised 72-hour fast.

    Why? It shows hypoglycaemia with inappropriately high insulin, C-peptide and proinsulin.

  21. A nurse has hypoglycaemia with high insulin but LOW C-peptide. What is the cause?

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    Exogenous (injected) insulin.

    Why? Pharmaceutical insulin contains no C-peptide and suppresses the patient's own. Insulinoma and sulfonylureas both give high insulin AND high C-peptide; a sulfonylurea screen separates them.

  22. Which oral drug is used to control hypoglycaemia from an insulinoma that cannot be resected?

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    Diazoxide.

    Why? It opens beta-cell K-ATP channels and inhibits insulin release. Somatostatin analogues are an alternative; surgery is definitive.

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