This man has SIADH (syndrome of inappropriate antidiuretic hormone) which is likely caused by a paraneoplastic syndrome associated with small cell lung cancer (FA2020 p228)
This man presents with hyonatremia, hypochloremia, normal potassium, normal BUN and creatinine, decreased plasma osmolality, and increased urine osmolality. SIADH is characterized by urine osmolality>serum osmolality and hyponatremia (p338). This is because ADH triggers retention of water by insertion of awuaporins into the collecting tubules. The increased body water triggers decreased secretion of renin and decreased activation of the renin-angiotensin-aldosterone system. Less aldosterone leads to less retention of sodium and less excretion of potassium. This combined with dilution from retention of water leads to hyponatremia with potassium normal. BUN/creatinine are unaffected because the kidneys are undamaged.
This is NOT ectopic ACTH secretion because that would lead to Cushing's syndrome which does not have the characteristic osmolality differences and increased cortisol can mimic mineralocorticoids leading to hypernatremia.
taylor5479In your last point, you referred to cushing's syndrome. I could be wrong, but I was under the impression that excess ACTH also causes an increase in mineralocorticoid production, not that increased cortisol necessarily mimics mineralocorticoids. Either way, it would result in the same effect of hypernatremia. +
chj7I think aldosterone production is mainly regulated by RAAS, while ACTH has major effects on glucocorticoid production and minor/tonic effects on aldosterone production (forgot where I saw this exactly, maybe UW?)+
submitted by โcassdawg(1780)
This man has SIADH (syndrome of inappropriate antidiuretic hormone) which is likely caused by a paraneoplastic syndrome associated with small cell lung cancer (FA2020 p228)
This man presents with hyonatremia, hypochloremia, normal potassium, normal BUN and creatinine, decreased plasma osmolality, and increased urine osmolality. SIADH is characterized by urine osmolality>serum osmolality and hyponatremia (p338). This is because ADH triggers retention of water by insertion of awuaporins into the collecting tubules. The increased body water triggers decreased secretion of renin and decreased activation of the renin-angiotensin-aldosterone system. Less aldosterone leads to less retention of sodium and less excretion of potassium. This combined with dilution from retention of water leads to hyponatremia with potassium normal. BUN/creatinine are unaffected because the kidneys are undamaged.
This is NOT ectopic ACTH secretion because that would lead to Cushing's syndrome which does not have the characteristic osmolality differences and increased cortisol can mimic mineralocorticoids leading to hypernatremia.