Low BP is sensed in glomerulus trigger of _____ from JG cells
catalyzes of cleavage of Ang I from angiotensinogen the to ang II via
How does Ang II increase BP
causes vasoconstriction and increaes aldosterone release from the zona glomerulosa of adrenal cortex
Aldosterone works in dista tubule to affect Na and K balance.. Aldosterone will ______ Na+ thus get retnetion of Na in body. In response, K and Hyrogen will be _____ in the tuble
leads to overall:
thus K and H will get secreated
end up with fluid retention and increased blood volume
drug to inhibit renin that works to decrease renin activity, but will see increased renin protein consentrtaions
Adrenal glands (from adenoma or one adrenal or both adrenals w/ hyperplasia) secreate excessive aldosterone that is AUTONOMOUS and not being controlled by:
renin and ang II
should see negative feedback as aldosterone increases
What is a result of excessive aldosterone
increased urinary potassium loss and hypertension (d/t excessive Na+ and fluid retention) with clinical presentation of Hypertension and Hypokalemia
Hypertension and Hyperkalemia are often seen in
pt comes in with Low K and high BP... what should we do?
consider test for primary hyperaldosteronism
also: resistant HTN, adrenal incidentaloma and HTN; onset of THN at young age <30 yr
We are thinking our patient has secondary hypertension, what kind of testing should we look into?
Morning blood sample in seated ambulant patient:
-Plasma aldosterone concentration (PAC)
Plasma renin activity (PRA) or plasma renin concentration
To make Dx of primary hyperaldosteronism, measure an incresaed ratio of:
Plasma Aldosterone : Plasma Renin (with potassium replete)
Aldosterone increasesd in pirmary hyperaldosteronism due to:
autonomous secreation from adrenal adenoma
Why is renin suppressed in pirmary hyperaldosteronism?
suppressed dt increaed blood pressure (baro reflex) and increased sodium (from increased reabsorption)
Pt has HTN and HYPOkalemia
see pt with resistant HTN
early onset HTN or very severe HTN
all signs of
What levels would we see to confirm primary aldosteronism:
PAC (plasma aldosterone concentration) and
PRA (plasma renin activity)
see HIGH aldosterone and LOW renin
Aldosterone:Renin ratio > 20
Aldosterone secreating adrenocortical adenoma adn bilateral hyperplasia of Zona Glomerulosa can cause:
Renal ischemia, decreased intravascular volume, CHF, chrnoic diuretics, hypoproteinemic states, Na-wasting disorders and chronic renal fail can all cause:
Renin ischeia increases renin secreation from:
CHF increases renin secration via:
Diuretic/laxatives increase renin because of
sodium and volume loss
ONce a dx of primary adlosteronism has been made you need to determine if this is from unilateral or bilateral adrenal source... what do we order?
CT scan of adrenal glands or AVS or sampling of what the adrenal glands are draining
The result of excess aldosterone produciton in response to increased RAAS activity
What do we use to distinguish difference between primary and secondary hyperaldosteronism
Renin levels increase in secondary forms where as in primary renin decresaes
What needs to happen before we do a scan to determine cause of hyperaldosteronism?
need to have a biochemical confirmaiton
You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a unilateral adrenal tumor... what is the treamtement?
You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a bilateral adrenal abnormality... what is the next step?
Perform a selective venous catherteriszation for aldosterone and cortisol to see if you can identify source: if unilateral do adrenalectomy
if bilateral, you can't take out both adrenals, thus do medicla management
What medicaitons are used to mange pts with bilateral hyperaldosteronism?
need to block aldosterone at the level of the receptor:
spironolactone or eplereonone
MOA of spilarinone or eplereinone
Competitive receptor antagonists of aldosterone
result in decreasing Na dn water retention and increase serum potassium
Glycyrrhizic acid can decrease activity of what enZ?
11-HSD2 ; see hypertention and hypokalemia
caused by 11HSD2 impairment thus dont convert cortisol to cortisone and increase cortisol action on the mineralcorticoid receptor in the kidney (mimics aldosterone)
Apparent mineralcorticoid excess
AME causes what symptoms?
Hypertention and hypokalemia, metabolic alkasosis, low renin acitivty, normal plamsa cortisal levels
Pt is prsenting like they ahve primary hyperaldosteronism but lack high aldosteorne levels
Cuase of Liddle syndrome
mutation in amiloride-sensitizing epithelial Na channel thus see increased activity of Na channel and increase Na reabsorption, K+ wasting, HTN and Hypokalemia
What do pts with Liddle sydrome have as far as renin and aldosterone levels?
What is our most importatn protector from hyperkalemia
as K increases, so does aldosterone to get rid of it