If diabetes insipidus was the lack of ADH,
let’s do the opposite.
So, here we have SIADH.
Now, before I go on though, I want to make
sure we are clear about one thing.
“Dr. Raj, we didn’t talk about nephrogenic
Oh yes, we did.
We did that in nephrology.
So, if you want your full explanation and
discussion of nephrogenic diabetes insipidus,
please refer to nephrology where there, we-we
referred to the receptors not working properly.
And so, therefore, you will also will have
polyuria and polydipsia.
But, in that case, you would then have ADH
levels being quite high because their receptors
Here we have SIADH.
Your patient with SIADH, who is he or she?
Well, if there’s SIADH, maybe perhaps that
surgery that I keep referring to, the transphenoidal,
there’s every possibility that you might
be releasing too much ADH from the posterior
Keep that in mind.
Or there might be drugs such as Carbamazepine
in which it may then result in increased release
of ADH or you could be paraneoplastic.
For example, a lung cancer that you should
know of known as small cell lung cancer, huh,
may result in increased release of ADH.
Welcome to syndrome of inappropriate anti-diuretic
Most will then appear as being asymptomatic,
that’s important, and here, because you’re
diluting your plasma, you are going to then
result in hyponatremia.
So, before we move on with SIADH, whatever
the cause may be, here the plasma osmolality
will be low and urine osmolality will be incredibly
You’re going to be forming concentrated
urine, aren’t you?
Now, what’s also important is the following.
Even though you’re reabsorbing this water…
reabsorbing this water… reabsorbing this
water, this comes back to our definition of
transudate and exudate or more or less what
it means to have transudate.
Remember, transudate to you should mean edema.
When we talk about edema, you’re referring
to the fact that we have accumulation of fluid
in your interstitium, don’t you?
This is my question to you.
Transudate, fluid in the interstitium, is
there sodium in transudate?
Yes or no?
Yes, yes, yes.
What is decrease in transudate is?
Why am I bringing this up to you?
This “edema” that you’re going to find
with SIADH, is it filled with sodium?
No, it’s not.
So, an important distinction point is the
Why am I bringing this up?
Because clinically... because this is not
fun to know, you actually need to… this
is fun to know, but clinically, why is it
A patient walk in with SIADH, when you know
that that patient has edema and you try to
press upon the skin to-to demonstrate pitting
edema, you’re not going to find it.
So, the exact mechanism, well, there are many
theories out there, but you’ll have what’s
known as euvolemia here, euvolemic, meaning-meaning
to say your patient with... have edema, but
it won’t be pitting, won’t be pitting
because it is not filled with sodium.
That’s something important for you to figure
out because if you’re thinking transudate...
remember right-sided heart failure with peripheral
pitting edema or when you have nephrotic syndrome
and you lose all that protein and that’s
your transudate, right?
Those are pitting edemas.
Here, you won’t find that.
I mention it here, if you’re a little confused
that’s okay because as we go through this,
that particular point will be solidified.
Symptoms - severe hyponatremia thus lethargic,
seizures and coma.
Now, hyper or hyponatremia, you will have
Usually seen with acute reductions in serum
Seen as disorders with SIADH.
Now, keep in mind, trauma, we saw both with
diabetes… central diabetes insipidus and
Comes back to that point, if you destroy that
posterior pituitary, there’s every possibility
that here, you might be releasing too much
And in the end, you might completely deplete
your posterior pituitary resulting in what,
Good, central diabetes insipidus.
If you are unfamiliar with that spectrum prior,
make sure that it is perfectly clear now.
With that said, take a look – stroke, trauma,
haemorrhage, infection, psychosis.
The second phase.
The first and second phase are the triphasic
event during that neurosurgery.
I’m not going to go through this one more
time, I’ve talked about this plenty.
Thoracic disease, this is a big one.
You find many a surgeons, in which especially
thoracic surgeons, when they’re performing
this whatever procedure for thoracic surgery
that the patient may present with SIADH.
Present with what?
Plasma osmolality elevated, concentrated urine.
Pneumonia, HIV patients with pneumocystis…
bacterial, viral, TB; pneumonia may often
present with SIADH.
I want you to put together pneumonia and thoracic
disease together and whenever there is either
surgery/invasive or pneumonia/infection, your
patient may present with SIADH.
There are theories out there, but for the
most part, you remember even the lung with
cancer with small cell may result with SIADH.
So, different things in the thoracic region
often associated with SIADH.
Drugs result in SIADH.
SSRIs, chlorpromazine, carbamezapine, high-dose
It’s a list that you want to make sure that
you memorize before taking your boards.
Other causes of SIADH.
Hereditary gain of function mutation.
Alright, so, we’ll take a look at this.
Here, it behaves like SIADH.
You can have loss of function or gain of function.
If it’s loss of function, before we move
on, take a look at the receptors that we have
here, arginine vasopressin V2 receptors, arginine
vasopressin V2 receptors.
Where are these receptors located?
If it’s loss of function of the receptors,
what’s your diagnosis?
Nephrogenic diabetes insipidus.
If it’s gain of function, it behaves like
SIADH; urine here is going to be concentrated.
These are type of questions that you’re
going to get on your boards, absolute thinking
How common is this?
Not very common, but what, do the boards love
Oh yeah, they do because it’s asking you
about gain and loss of function, completely
changing your presentation and diagnosis of
Here’s ectopic ADH, where?
Small cell lung cancer, a type of bronchogenic