Step 1: State the physiology that has gone wrong:
In SIADH, ADH is released without the right stimulus. This time the source is a lung tumour.
Too much ADH means too much water is reabsorbed. The blood sodium falls because of dilution, and the urine stays concentrated.
Step 2: Decide what a good drug must do:
A good drug here should either stop ADH acting on the kidney or help the kidney lose free water.
A drug that adds more ADH action, or that wastes sodium along with water, would be a poor match.
Step 3: Apply this to each choice:
Desmopressin acts like ADH. It would add to the problem, so it is the opposite of what we want.
Thiazide diuretics block sodium chloride transport in the distal tubule. They reduce the ability to dilute urine and often cause hyponatraemia. They are used in nephrogenic diabetes insipidus.
Furosemide is a loop diuretic. It is used only as an add-on, along with salt tablets, and it is not a specific treatment.
Tolvaptan blocks V2 receptors, so it directly cancels the excess ADH.
Step 4: Understand how tolvaptan works:
Tolvaptan blocks the V2 receptor on the basolateral side of the collecting duct cell. Aquaporin-2 is no longer placed in the apical membrane.
Water stays in the urine and is passed as dilute urine. Serum sodium then rises.
Monitoring is needed, because a fast rise in sodium can cause osmotic demyelination. Liver function should also be watched with long-term use.
Step 5: Other measures to remember:
Fluid restriction is the first line. Demeclocycline causes nephrogenic diabetes insipidus and is another option. Hypertonic saline is used when seizures or coma are present.
Final Answer:
Tolvaptan, a V2 antagonist, is the drug that can be used in this patient. This is option (B).