Syndrome of inappropriate antidiuretic hormone (SIADH)

Syndrome of inappropriate antidiuretic hormone (SIADH)

What is SIADH? How does your body know when to retain fluids
and when to get rid of them? It’s not like you just think to yourself “I’ve had too
much water, better get rid of some.” (If you do, and it works, call us). Your body
uses chemicals called hormones to send widespread messages, kind of like how the P.A. system
at school tells everyone to ignore the smoke billowing out of the science wing. The antidiuretic hormone, abbreviated as ADH,
is the hormone that controls water retention in the body. It also constrict blood vessels,
and incidentally the vasoconstrictor drug called vasopressin is just ADH. Cool! But
that’s not what we’re talking about right now. Anyways, the more ADH floating around
in your blood, the more fluid you retain. The less ADH in your blood, the more fluid
you excrete. The nephrons in the kidneys are the structures
that physically control how much water is excreted from your body. Nephrons are mostly
a series of tubes attached end-to-end that type fluids and wastes towards the bladder.
These tubes though also allow fluids and electrolytes to move through the tube walls and back into
the blood if needed. ADH affects the last two-thirds of these tubes, called the distal
convoluted tubule and the collecting ducts. These tubes focus almost exclusively on reabsorbing
water back into the blood. The wall of these tubes are unsurprisingly made up of cells,
a common trait of living things, but these cells have proteins called aquaporins. Aquaporins
allow water to move quickly in and out of the cells. The more ADH floating around in
the blood, the more aquaporins are available to… ahem…facilitate water movement through
the cell (yo, wata, come over here for a sec). So when ADH is low, most of the water flows
through the the distal convoluted tubule and the collecting duct, giving us diluted urine.
When ADH is high, aquaporins grab much of the water passing through the these tubes
and throws them back into the blood. When I drink a glass of water and that water
is absorbed into my blood, my plasma osmolality drops, which means I’m diluting my blood
with the water. That means there’s more fluid for all those blood cells to bounce
around in (wooo parrttayy). The part of my brain called the hypothalamus sees this drop
in plasma osmolality and tells the pituitary gland to slow down the release of ADH (that’s
enough!). Low ADH leads to lots of diluted urine (urine with low osmolality), which brings
our plasma osmolality back to normal. What a nifty feedback loop. Now suppose ADH continues to be released even
though my plasma osmolality has dropped (stop it! STOP IT! pituitary gland whistling). We’re
going to continue retaining water, and as we drink more and more water, we might expect
our plasma osmolality to continue dropping. However this isn’t exactly the case. As
more water is retained, it dilutes the other solutes floating around in our blood, like
sodium. The extra fluid also takes up more space in our blood vessels. This taking up
more space issue triggers another mechanism in our body that causes the hormone aldosterone
to stop being released. Less aldosterone floating around in the blood causes the body to start
dumping sodium from the blood into the urine. Concentration gradients cause water to follow
sodium, so we end up with the excess water being excreted in the urine with the sodium,
normalizing the fluid volume in the blood. So now our body is removing sodium from blood
that already has a lower concentration of sodium. Uh oh! This means the plasma sodium
osmolarity is dropping significantly. This whole fiasco we’ve just talked about is
called syndrome of inappropriate antidiuretic hormone, often abbreviated as SIADH. There are four patterns of ADH release in
people with SIADH. Type A is completely erratic and is independent
of the plasma osmolality. ADH levels tend to be very high so the maximum amount of fluid
is retained, causing urine osmolality to be very high.
Type B is a constant release of a moderate amount of ADH.
Type C is the “baseline” plasma sodium concentration level is set lower than normal.
It’s like you turned down the thermostat in your house to a new lower level. This type
is particularly unique because the plasma sodium concentration is stable, unlike other
SIADH’s where it would continue to fall. Type D is the least common type of SIADH where
ADH secretion is completely normal, yet urine osmolality is still high. The symptoms a person with SIADH experiences
is caused by the dilution and loss of sodium in the blood. When your body has a lower sodium
concentration than normal, you experience symptoms similar to dehydration or any other
condition where sodium is low. Symptoms like headaches, nausea, and vomiting are common
initially, along with muscle cramps and tremors. As the sodium concentration continues to get
lower in your blood, the neurons in your brain begin to swell leading to cerebral edema.
This causes symptoms like confusion, mood swings, and hallucinations. If left untreated
it will lead to the common downwards trend in most illnesses of seizure, coma, death. It’s not too hard to suspect someone might
have SIADH. All we have to do is consider your symptoms in addition to your lab results.
Low blood sodium levels and low plasma osmolarity combined with high urine osmolality and high
urine sodium is a giant red flag for SIADH. So what causes SIADH? Pretty much anything
that messes with the secretion of ADH. Conditions like strokes, hemorrhages, or trauma
to the brain can mess up the brain’s ability to release ADH.
Similarly, some drugs that act on the brain like mood stabilizers or anti-epileptics can
change the way ADH is released. Surgery in general often causes an increase
secretion of ADH, although we’re not entirely sure why. Obviously brain surgery, specifically
to the pituitary gland also might cause extra ADH to be released.
ADH can also be produced ectopically by tumors, which means the tumors themselves produce
ADH outside of the pituitary gland and release ADH into the bloodstream. Small cell carcinoma
in the lungs is the type of cancer most likely to release ADH this way.
Infections in the lungs and brain are also linked to increase the risk of ADH secretion.
If some of your family members have had SIADH before, there’s also a possibility you may
develop it. The best treatment for SIADH is to figure
out what the underlying cause of the excessive ADH is, and treat that problem. Otherwise
we can manage SIADH by restricting your daily intake of fluid. You can also start a high-salt
and high-protein diet to help replace the excess loss of sodium. Drugs that inhibit
ADH secretion can also be used in chronic SIADH situations. For people who have really
severe acute hyponatremia symptoms, hypertonic IV fluids are usually administered.


  1. So excuse me, I am uneducated, but could SIADH actually cause hyperhydrosis or even CSF leaks because your body is desperately trying to get ride of excess water but It is unable to through the urine?

  2. 3:26~3:35 The "uh oh" and "this whole fiasco we've just talked about…" made me giggle, it sounds so funny when the speaker says it, i don't know why.

    EDIT/ADD: ~6:13 Bloody 'ell that smilie on the tumour is just genius! X'3

  3. I loved it, thank you so much, it helped me with my biochemestry final.
    It is very understandable, entertaining and complete.

  4. The 'uh-oh' drove home the point. 😉
    Great explanation, always thought SIADH was very muddled up, until I watched this. Thanks!

  5. Great job osmosis once again! But why does hyponatremia cause muscle cramps? I know that muscles cramps are due to impaired detachment of myosin from actin. So how does sodium affect that? 🙂

  6. How many times can we LIKE this video. ive watched it 3x and now can recite it verbatim and actually did to my classmates. GREAT video. Just the right length, speech speed (sometimes ppl speak so slowly im in a coma before 10min video ends other times they race thru it i feel like WTH just happened and have to keep stopping and rewinding. not the case in your videos, THANKS)

  7. one thing was mentioned wrongly, lithium might be used to treat SIADH, rather than causing it. Lithium causes diabetes insipidus.

  8. The subtle humor in this excellent video is great. "…is, unsurprisingly made up of cells, which is a common trait among living things…" Thank you so much!

  9. My heart sinks whenever i look up a medical video and osmosis isn't among the options. yes, osmosis videos are that amazing.

  10. this is the equivalent of reading a textbook for one hour (in terms of content/my retention of material) and i love you guys for it.

  11. all of ur videos are very very useful for med students. can't thank u enough. great effort, presentation and description. love u osmosia. glad i found u ❤

  12. A person with SIADH cannot have hypovolemia, dehydration or features of fluid overload. SIADH hyponatremia is Hypo osmolar Euvolemic hyponatremia.
    (For diagnostic/exam purposes)

  13. You said that the decrease in serum osmolality will dilute sodium, then how about other electrolytes in the body? Will they be diluted as well(like potassium)?

  14. Very clear explanation. CHF exacerbation is not listed as a cause, but by my understanding is both relatively common and clinically important to understand in relation to SIADH

  15. Great video! Very well explained – some more info on paraneoplastic syndromes associated and the consequences of rapid overcorrecting of sodium would be useful for future viewers :)!

  16. Never dissapointing it.. Can u add on more video about endocrine patho please such as diabetes insipidus, hypopituit, hyperpit etc 🙂

  17. Actually I do have a question. At 3:00 you say that aldosterone it's responding to hypertension (increased fluids in the circulatory system) by dumping the water and the Na in the urine. What I was wondering is that, isn't Aldosterone released when the flow in the bloodstream is low? which "activates the basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid"-Wikipedia? So, how does Aldosterone make the Na levels worse?(Besides that, it has other functions to try to maintain Na levels normal)


  19. I am a bit confused as to why there is Low Aldosterone. aldosterone works to increase Sodium re-absorption, when this is low sodium around… correct? so in this case, if there is dilute blood (more water than Sodium) wouldn't this cause aldosterone to be released?

  20. Excellent video, as always! Could you also upload one on Diabetes Insipidus please? None of the other Youtube videos explain it like you do. Thanks!

  21. Thank you so much Osmosis, you guys are best, you have taught all the difficult topic with so much easy understanding. And all points covered are very clinically relevant and can be used in daily patient care. I am just loving these. Its really helping to brush up my concepts

  22. Hi…if it takes more space then that means the strech receptors are stimulated that means there should be more aldosterone but you said aldosterone decresases when fliud takes more space..please do reply

  23. SIADH = Antidiuretic Hormone? Si (Yes).

    Not much substance there, but I use such tricks. There’s a whole wide world of information out there. Efficiency matters.

Leave a Reply

Your email address will not be published.