If patient -only- had hypertension: ACTH more likely than SIADH.
Patient with hypertension AND hypokalemia: 100% ACTH.
Don't feel bad friends, I also had this question wrong :(...
To rule out SIADH type: "Serum potassium concentration generally remains unchanged. Movement of potassium from the intracellular space to the extracellular space prevents dilutional hypokalemia. As hydrogen ions move intracellularly, they are exchanged for potassium in order to maintain electroneutrality."
epi = pheochromocytoma of adrenal medulla = episodic HTN PTHrP = squamous cell carcinoma of lung (plus others) = hypercalcemia VIPoma = neuroendocrine pancreatic tumor =secretory diarrhea [WDHA (watery diarrhea, hypokalemia, achlorhydia]
Aldo is primarily regulated by ATII. Cortisol is primarily regulated by ACTH. However, since cortisol can also activate aldo secondarily, it works. However, I believe that ADH should not have been answer choice however since no lung biopsy findings were reported so we can't really distinguish between SCC vs. NSCLC
AT-II is the main stimulator of aldosterone release. This is kind of bull shit because that was the answer to one of the other NBME questions in ACTH cushing's disease "wHaT pArT oF tHe GlAnD iSn'T eNlArGed?"
submitted by โneonem(629)
Small cell carcinoma of the lung may produce paraneoplastic syndromes, of which ACTH and ADH are the more common subtypes. ACTH excess leads to excess stimulation on the adrenal cortex to produce cortisol, resulting Cushing's syndrome. Excess cortisol (normally a stress hormone) causes hypertension via potentiation of sympathetic stimulation on the vasculature. It can also cause hypokalemia by acting as a mineralocorticoid when in excess, saturating the ability of 11-beta-hydroxysteroid dehydrogenase (present in the renal tubules) to convert cortisol to cortisone, which doesn't act as a mineralocorticoid.