Hyperaldosteronism – causes, symptoms, diagnosis, treatment, pathology

Hyperaldosteronism refers to an endocrine
disorder where the adrenal gland produces above normal levels of the hormone aldosterone. Now, there are two adrenal glands, one above
each kidney, and each one has an inner layer called the medulla and an outer layer called
the cortex which is subdivided into three more layers, the zona glomerulosa, zona fasciculata,
and the zona reticularis. The outermost layer is the zona glomerulosa,
and it’s full of cells that make the hormone aldosterone. Aldosterone is part of a hormone family or
axis which work together and are called the renin-angiotensin-aldosterone system. Together these hormones decrease potassium
levels, increase sodium levels, and increase blood volume and blood pressure. Aldosterone is secreted in response to elevated
levels of renin, and it’s role is to bind to receptors on two types of cells along the
distal convoluted tubule of the nephron. First it stimulates the sodium/potassium ion
pumps of the principal cells to work even harder. These pumps drive potassium from the blood
into the cells and from there it flows down its concentration gradient into the tubule
to be excreted as urine. At the same time, the pumps drive sodium in
the opposite direction from the cell into the blood, which allows more sodium to flow
from the tubule to the cell down its concentration gradient. Since water often flows with sodium through
a process of osmosis, water also moves into the blood, which increases blood volume and
therefore blood pressure. The other function of aldosterone is to stimulate
the ATPase pumps in alpha-intercalated cells which causes more protons to get excreted
into the urine. Meanwhile, ion exchangers on the basal surface
of the cell move the negatively charged bicarbonate ion into the extracellular space, causing
an increase in pH. Hyperaldosteronism can happen due to primary
causes which is where the adrenal gland itself is responsible for the excess production of
aldosterone. The most common primary cause is called idiopathic
hyperaldosteronism, because the zona glomerulosa has an increase in the number of cells secreting
aldosterone, but it’s not really clear why this happens. The second most common cause is called Conn
syndrome and this is where an adenoma or tumor in the glandular epithelial cells secretes
too much hormone. A third cause is familial hyperaldosteronism,
and this is a genetic condition that runs in families, and it’s when the zona glomerulosa
cells inappropriately make aldosterone in response to adrenocorticotropic hormone which
is secreted by the pituitary gland, and this is in addition to responding to renin as normal. Hyperaldosteronism can also be due to secondary
causes where the pathology lies outside of the adrenal gland. Secondary causes of hyperaldosteronism are
usually due to excess aldosterone production in response to high levels of renin. This might happen when there’s a chronic
decrease in blood pressure like in congestive heart failure or cirrhosis. Hyperaldosteronism leads to hypokalemia, which
is low potassium levels in the blood, as well as hypernatremia—high sodium levels in the
blood. With more sodium around in the blood, water
moves into the blood vessels, which results in a high blood volume and high blood pressure,
or hypertension. Finally, the loss of protons also results
in an alkalosis, and more specifically a metabolic alkalosis, since it’s caused by the kidneys. Individuals with hyperaldosteronism typically
develop hypertension related symptoms like headaches and facial flushing, as well as
hypokalemia related symptoms like constipation, weakness, and potentially changes in their
heart rhythm. The diagnosis of hyperaldosteronism is mainly
done by measuring levels of renin and aldosterone. In primary hyperaldosteronism, the main problem
is that zona glomerulosa cells secrete high levels of aldosterone, and that aldosterone
has a negative feedback effect on renin, and so it actually inhibits renin production. So in this case aldosterone levels are high
and renin levels are low in. In secondary hyperaldosteronism, on the other
hand, the main problem is that there is too much renin produced by the juxtaglomerular
cells of the kidneys, so even though aldosterone’s inhibiting renin secretion, renin production’s
still being stimulated by those cells, and this means that there’s both high levels
of aldosterone and high levels of renin. Treatment of hyperaldosteronism is usually
with potassium-sparing diuretics, especially spironolactone, which competitively binds
to aldosterone receptors on the principal and alpha-intercalated cells. With these medications around, aldosterone
can’t exert its effects. Additionally, treating the underlying cause
can be helpful. For example, in Conn syndrome surgical removal
of the tumor can help, and also managing heart failure and cirrhosis. All right, as a quick recap, hyperaldosteronism
is the chronic, excess secretion of aldosterone from the zona glomerulosa of the adrenal gland,
and these high aldosterone levels can lead to hypokalemia, hypernatremia, hypertension,
and a metabolic alkalosis. Thanks for watching, you can help support
us by donating on patreon, or subscribing to our channel, or telling your friends about
us on social media.

82 comments

  1. Thanks for osmosis for clearing us from difficult concepts..One request from me…can you make a video about Hyperparathyroidism and neoplasia? 😎

  2. Hi thanks for the video, I just had a question about why hyperalderstonism leads to Alkalosis….

    If the presence of Aldersterone causes an up regulation in the ATPase (in intercalated cells) which thus increases the H+ ions lost would that not cause more HCO3- to be drawn into the intercalated cells (rather than out) to balance out the change in charge?

    Many thanks

  3. Quick Question regarding this video: Could you explain the Hypernatremia? I thought it is only transient. Isn't there an Aldosterone Escape Mechanism that causes an increased total body sodium but not sodium concentration (because of water reabsorption?). Leading to increased naturesis and diuresis but no edema?

  4. hmm Dr. Sattar says 1) adenoma 2) sporadic ….also in primary aldosteronism all of those lab values will not be presented (low renin, high bnp.. aldosterone escape)

  5. Please check regarding the Familial hyperaldosteronism. Its a primary hyperaldosteronism not due to increased ACTH (which represents a secondary cause) Instead its due to aldosterone synthase overactivity, and potassium channel defect. https://ghr.nlm.nih.gov/condition/familial-hyperaldosteronism#genes

  6. I'm 30, have a pituitary adenoma, cyclically elevated cortisol levels and an aldosterone level 5x the high end of the normal range. I've been on diuretics for a good ten years now and I've been sick my entire life. I still cannot get any doctors to figure out what's going on because they refuse to admit the tumor is the problem and take it out. I have en endocrinologist telling me the tumor isn't causing the high aldosterone it might be the diuretics.. and a nephrologist telling me absolutely the tumor is the problem and not the diuretics so… can a pituitary adenoma be a secondary cause of high aldosterone levels? 20 years and I still can't get any help. I'm probably going to die from this shit before they figure it out. I'm just a prime example of how not every patient is by the book. It should be a lesson for all medical professionals.

  7. I thought principal and alpha cells were on the collecting duct, not the DCT. Which one is it? I got my information from USMLE First Aid 2017

  8. Ur videos are awesome… Bt as far as medical pathology is concerned we need more gross and microscopic features of every disease…if u cud include dat too…it would be jst fantastic

  9. Hey osmosis team! I wanted to ask you; does the osmosis prime member subscription provide study plans only for USA med students? I’m studying medicine in Europe and I would like to know what prime member subscription offers to us 🙂 thanks

  10. Thank you for all the awesome videos! I'm a nursing student, and although some of the advanced details of the pathologies aren't all that important (at least when it comes to test-taking), I think understanding the diseases helps me greatly because I can think through the questions, rather than trying to remember pieces of information that have little meaning.
    Also, I would appreciate it greatly if you guys can make the Hyper/Hyponatremia videos! Looking forward to more great videos!

  11. According to McGraw-Hill new addition App for Board Recertif. ( I am doing this and ABFM review and listening to you U-tube videos, the primary cause of Primary Hyperalderonism is Conn's then Idiopathic. So now I need to go to a third reference to see if I can find the answer since Boards on are in 10 days. I am a practicing phyisican out of school over 15 years and this is my last time I have to recertify. In all my years of practicing, I have never seen Conn's or any other type of hyperaldosteronism.

  12. TYPES OF PRIMARY ALDOSTERONISM — Renin-independent, incompletely suppressible (primary) hypersecretion of aldosterone is an increasingly recognized but still underdiagnosed cause of hypertension [1]; it is estimated to be responsible for 5 to 13 percent of hypertension in humans. Many subtypes of primary aldosteronism have been described since Conn's original report of the aldosterone-producing adenoma (APA) in 1954 [2-5].

    The most frequent causes of primary aldosteronism include:

    ●Bilateral idiopathic hyperaldosteronism (or idiopathic hyperplasia [IHA], 60 to 70 percent)

    ●Unilateral APAs (30 to 40 percent)

    This is from Up To Date, FYI

  13. Conn syndrome and bilateral adrenal hyperplasia are not the same thing, right? I think you have to have an adenoma to have Conn syndrome. Also, I guess you could use eplerenone instead. Spironolactone causes more gynacomastia.

  14. big love ❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️
    this was amazing 😘😘😘😘😘😘

  15. Has anyone here had Adrenal Vein blood sampling? I'm due to have this procedure to find out why my aldosterone levels are so high and want to know what to expect. Thanks.

  16. i watched this video to understand the concept of aldosterone escape mechanism but first time osmosis channel disappointed me…as even no context of escape mechanism i found here….

  17. I have like this renin and and the normal is 2.8 but mine is 500
    So from that i have hypertension i really hope i get better my doc seas it id only from puberty and it will go eventually

  18. Na+ concentration should be normal because of ANP actions (b/c fluid overload) which causes normal Na+ level by netriuresis.
    -escape phenomenon

  19. Was put on bp meds last 3 years
    🤦‍♀️🤦‍♀️🤦‍♀️
    Thank you so much for this video 😍😍😍😍👍👍👍🙂🙏🙌❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️❤️

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