Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.
Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).
I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?
briseWouldn't that be more long term?+12019-06-12T17:07:36Z
sugaplumI think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia. +2019-06-23T00:46:05Z
davidwShe has Fibromuscular dysplasia which should be in your differential for a young female with hypertension ( along with Conns syndrome and pheochromocytoma). it typically causes stenosis and aneurism formation of the renal arteries leading to elevated renin. +22019-07-06T19:09:41Z
to snoo-finity ... and beyond!
submitted by mcl(375), 2019-06-07T20:54:03Z
Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.
Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).
I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?