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ADH, SIADH & diabetes insipidus flashcards

16 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. Through which receptor and second messenger does ADH cause water reabsorption in the kidney?

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   V2 receptor, via adenylate cyclase/cAMP, causing insertion of aquaporin-2 channels in the collecting duct.

   Why? Aquaporin-2 lets water move out of the collecting duct, concentrating the urine.

2. Terlipressin is used for oesophageal variceal bleeding. Which vasopressin receptor does it act on?

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   V1 receptors, causing splanchnic vasoconstriction.

   Why? Splanchnic vasoconstriction lowers portal inflow and so portal pressure.

3. Why can desmopressin be used in mild haemophilia A and von Willebrand disease?

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   It acts on extra-renal V2 receptors on vascular endothelium to release von Willebrand factor and factor VIII.

   Why? The released vWF and factor VIII temporarily raise their plasma levels enough to cover minor bleeding or procedures.

4. Name three drugs that can cause SIADH.

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   Any three of: SSRIs, carbamazepine, sulfonylureas (also other antidepressants and antiepileptics).

   Why? These drugs increase ADH release or its effect on the kidney, so free water is retained.

5. In a euvolaemic patient with hyponatraemia and low plasma osmolality, which urine results support SIADH?

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   Urine sodium >20 mmol/L and urine osmolality >100 mOsm/kg (inappropriately concentrated).

   Why? SIADH needs normal adrenal, thyroid and renal function to be confirmed before the diagnosis is made.

6. What is the first-line treatment for mild-to-moderate chronic SIADH?

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   Fluid restriction (about 800–1000 mL/day), plus treating the cause.

   Why? Restricting free water intake lets the kidneys slowly raise the sodium.

7. What is the mechanism of action of tolvaptan?

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   Selective vasopressin V2 receptor antagonist (a "vaptan").

   Why? Blocking V2 causes aquaresis — loss of free water without sodium — so serum sodium rises.

8. Why is demeclocycline now rarely used for chronic SIADH?

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   It is nephrotoxic, and safer alternatives exist.

   Why? Demeclocycline works by causing a nephrogenic diabetes insipidus — it blocks the renal response to ADH.

9. What is the treatment of severe symptomatic hyponatraemia (e.g. seizures or coma)?

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   3% hypertonic saline: 150 mL IV over 20 minutes, repeated up to twice more until sodium has risen by about 5 mmol/L.

   Why? A small, controlled rise in sodium quickly reduces cerebral oedema. Give it whatever the cause of the hyponatraemia, with close sodium monitoring.

10. What complication follows over-rapid correction of chronic hyponatraemia, and which part of the brain is classically affected?

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    Osmotic demyelination syndrome, classically in the central pons (central pontine myelinolysis).

    Why? The brain has adapted to low osmolality; a rapid rise shrinks cells and causes demyelination. Signs (dysarthria, dysphagia, quadriparesis, locked-in) appear 2–6 days later.

11. What is the treatment for lithium-induced nephrogenic diabetes insipidus?

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    Amiloride.

    Why? Lithium enters collecting-duct cells through ENaC channels; amiloride blocks ENaC and so reduces lithium uptake.

12. Which drug class paradoxically reduces urine output in nephrogenic diabetes insipidus?

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    Thiazide diuretics (often with indomethacin).

    Why? Mild volume depletion increases proximal sodium and water reabsorption, so less water reaches the collecting duct.

13. In a water deprivation test, what urine osmolality after desmopressin indicates cranial DI?

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    Urine osmolality rises to >600 mOsm/kg.

    Why? The kidney responds normally to ADH in cranial DI. In nephrogenic DI the urine stays dilute (<300 mOsm/kg) after desmopressin.

14. Which electrolyte disturbance is a recognised cause of nephrogenic diabetes insipidus?

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    Hypercalcaemia (hypokalaemia can also cause it).

    Why? High calcium impairs the collecting duct response to ADH.

15. DIDMOAD (______ syndrome) combines diabetes insipidus (cranial), diabetes mellitus, optic atrophy and deafness.

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    Wolfram

    Why? It is a rare inherited neurodegenerative syndrome; the DI is central.

16. A man with schizophrenia drinks about 10 litres of water a day. Sodium is 122 mmol/L and urine osmolality is 60 mOsm/kg. What is the most likely diagnosis?

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    Primary (psychogenic) polydipsia.

    Why? Low sodium with maximally dilute urine means the kidneys are correctly excreting excess water.