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Old 06-17-2015
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Default Orthostatic HypEr-tension weird question in UW

Hi there guys
I came across a question in UW that describes a patient with high blood pressure and low renin, the diagnosis turned out to be Conn's syndrome

The weird part was that the patient's systolic blood pressure goes up (from 190 to 195) on standing; and his heart rate drops (from 72 to 70) also on standing. His diastolic blood pressure didn't change with changing position.

they didn't mention in the answers why that happened, and I really tried to find an explanation but no clue :/

any thoughts?
Thanks
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Khorreed (06-17-2015)



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Originally Posted by modamada313 View Post
Hi there guys
I came across a question in UW that describes a patient with high blood pressure and low renin, the diagnosis turned out to be Conn's syndrome

The weird part was that the patient's systolic blood pressure goes up (from 190 to 195) on standing; and his heart rate drops (from 72 to 70) also on standing. His diastolic blood pressure didn't change with changing position.

they didn't mention in the answers why that happened, and I really tried to find an explanation but no clue :/

any thoughts?
Thanks
I dont think that increase in bp by 5 mm is relevant in this case. You just look at the low renin.
In primary hyperaldesteronism Na reabsorbed more by principal cells of nephrone. H2O follows Na - higher ECF, plasma fluid and blood pressure. Then GFR is more because more blood volume - more pressure in Glomerulus arteriols. After filtration in bowmans capsule pressure is more - so more pressure in other parts of neprone(such as Distal Convulated Tubules). Speed of fluid is more - not all Na reabsorbed in proximal tubules(because of speed because of higher pressure of fluid in nephrone) so more Na coming to DCT where JGA is. JGA feels that NA is more so it turns off - less renin.
About systolic pressure. Maybe while standing more blood is in veins - so less blood in arteries - less GFR - less speed of fluid in nephrone - less NA in DCT - JGA slightly turned on(because it get used to higher pressure) - slightly more renin - more pressure in efferent arteriols of nephrone(because of Angiotensin 2) - more TPR(but TPR is only oppose dyastolic pressure, so I think I am wrong here)
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