SIADH -MCQs (PG / SS level)
1. Classic biochemical criterion for SIADH is:
SIADH is hypotonic hyponatremia — low serum osmolality (<275) with inappropriately concentrated urine is central.
2. Urine sodium in SIADH is typically:
Urine Na⁺ is usually elevated (>30–40 mEq/L) because kidneys excrete sodium despite hyponatremia.
3. Volume status in SIADH is best described as:
Patients are typically euvolemic—no clinical dehydration or frank edema.
4. Which lab helps distinguish SIADH from hypovolemic hyponatremia?
Urine Na⁺ is high in SIADH despite hyponatremia; in hypovolemia urine Na⁺ is low unless diuretics are used.
5. Low serum uric acid in hyponatremia suggests:
SIADH often has low uric acid due to increased renal excretion; in CSW uric acid may normalize after correction.
6. Fractional excretion of uric acid (FEUA) >12% favors:
FEUA >12% is supportive of SIADH (and can be elevated in CSW), but clinical context is key.
7. Most common paraneoplastic cause of SIADH is:
SCLC frequently secretes ectopic ADH causing SIADH.
8. Which drug is classically associated with causing SIADH?
Carbamazepine increases ADH release or renal sensitivity; other drugs include SSRIs, cyclophosphamide, vincristine.
9. In a patient with SAH and hyponatremia with clear signs of hypovolemia, the most likely diagnosis is:
CSW occurs after CNS injury (SAH, trauma) with renal salt loss and hypovolemia.
10. First-line management for mild, chronic SIADH is:
Conservative management with fluid restriction (and addressing cause) is initial therapy for mild SIADH.
11. Which agent causes nephrogenic DI-like effect used in SIADH treatment?
Demeclocycline induces renal resistance to ADH (nephrogenic DI effect); vaptans antagonize V2 receptors but work differently.
12. Vaptans (tolvaptan/conivaptan) act by:
They block V2 receptors, causing aquaresis (free water excretion) and raising serum sodium.
13. Rapid correction of chronic hyponatremia risks:
Overly rapid correction → osmotic demyelination; limit correction to safe rates (e.g., ≤8–10 mmol/L/day depending on guidelines).
14. In acute severe symptomatic hyponatremia with seizures, the immediate appropriate step is:
Severe symptomatic hyponatremia (seizures, coma) requires hypertonic saline bolus to rapidly increase Na⁺ by a small safe amount.
15. Which finding principally differentiates CSW from SIADH?
Volume status: CSW → hypovolemia (dehydration signs); SIADH → euvolemia. This is the central distinguishing feature clinically.
16. After administration of isotonic saline to a patient with SIADH, serum sodium usually:
Isotonic saline is often ineffective in SIADH because infused water is retained and sodium may be excreted — hypertonic solutions or aquaretics are needed in severe cases.
17. Which lab test result would you expect in SIADH?
SIADH: inappropriately concentrated urine (>100 mOsm/kg) despite low serum osmolality.
18. Which is a recognized adverse effect of demeclocycline?
Demeclocycline can cause renal impairment and photosensitivity; avoid in renal failure and use with caution.
19. Rapid initial correction target in severely symptomatic hyponatremia is to raise serum Na by:
Give small hypertonic saline boluses to raise Na by ~4–6 mmol/L to control severe symptoms; avoid overcorrection.
20. In chronic hyponatremia, safe maximum correction is generally considered:
To reduce ODS risk, chronic hyponatremia correction should be conservative (≤8–10 mmol/L in 24 h; exact target depends on risk factors).
21. The mechanism of hyponatremia in primary polydipsia is:
Primary polydipsia: dilute water intake exceeds kidneys’ ability to excrete free water, causing hyponatremia with very low urine osmolality.
22. Which of the following increases free water excretion (aquaresis) without major electrolyte loss?
Vaptans increase free water excretion, raising serum Na⁺ while largely sparing electrolytes (useful in euvolemic/hypervolemic hyponatremia).
23. Which diuretic class can paradoxically cause hyponatremia due to increasing ADH sensitivity?
Thiazides impair urinary dilution and increase ADH sensitivity, commonly causing hyponatremia.
24. Which is true about CSW management?
CSW requires volume and sodium replacement; fludrocortisone can help reduce renal salt loss.
25. In SIADH, measuring serum cortisol and TSH is important to exclude:
Adrenal insufficiency and hypothyroidism can mimic SIADH; they must be excluded prior to diagnosis.
26. Which pattern is likely in CSW compared to SIADH after sodium correction?
With correction of hypovolemia in CSW, uric acid typically normalizes; in SIADH it often remains low.
27. Which electrolyte abnormality commonly accompanies SIADH?
Low BUN and low uric acid are typical biochemical clues suggesting SIADH.
28. Which of the following is an indication for using vaptans?
Vaptans are used in euvolemic/hypervolemic hyponatremia resistant to conservative measures, not in hypovolemia.
29. Which physiologic response occurs in chronic hypotonic hyponatremia?
Chronic hyponatremia leads to cellular adaptation (loss of organic osmolytes) which reduces cerebral edema — reason for cautious correction.
30. Which condition is least likely to cause SIADH?
Primary hyperaldosteronism causes sodium retention and hypertension, not SIADH; pulmonary disease, malignancy, and drugs often trigger SIADH.
31. Which monitoring is essential when initiating vaptan therapy?
Vaptans can correct sodium rapidly; frequent serum sodium checks are required to avoid overcorrection. (Also check liver fx if long term tol vaptan.)
32. A patient on thiazide diuretic presents with hyponatremia — the likely mechanism is:
Thiazides impair urinary dilution in the distal tubule, promoting hyponatremia, especially in elderly or low-Na diets.
33. In SIADH, which of the following is usually low?
Low BUN reflects dilution and reduced urea production; urine sodium and urine osmolality are typically high in SIADH.
34. Which statement about hypertonic saline during hyponatremia treatment is true?
Small hypertonic saline boluses rapidly relieve life-threatening symptoms; careful monitoring prevents overcorrection.
35. Which hormone deficiency can mimic SIADH by causing hyponatremia?
Adrenal insufficiency (secondary) can cause hyponatremia due to reduced cortisol and increased ADH; check cortisol before diagnosing SIADH.
36. Which is a recognized risk factor for osmotic demyelination syndrome during correction?
Chronic alcoholism, malnutrition, and very low baseline Na increase risk of ODS if corrected too rapidly.
37. In suspected SIADH, which of the following measurements is least helpful?
Serum troponin is unrelated; urine osmolality, urine sodium, and cortisol (to exclude adrenal insufficiency) are relevant.
38. Which clinical scenario should raise suspicion for SIADH?
Drugs like SSRIs in elderly hospitalized patients commonly cause SIADH — look for euvolemic hyponatremia without edema.
39. Which of the following statements about CSW is TRUE?
CSW follows CNS injury and is marked by renal salt loss leading to hypovolemia — treat with volume and sodium replacement.
40. For exam-style reasoning: A euvolemic patient with Na 123, urine Osm 520, urine Na 70, normal TSH/cortisol — best next step?
Findings fit SIADH (euvolemic, concentrated urine, high urine sodium); initial management is fluid restriction and search for underlying cause.
