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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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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).
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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.
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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.
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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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