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SIADH: Clinical Presentation

by Carlo Raj, MD
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    00:03 If diabetes insipidus was the lack of ADH, let’s do the opposite.

    00:09 So, here we have SIADH.

    00:12 Now, before I go on though, I want to make sure we are clear about one thing.

    00:16 “Dr. Raj, we didn’t talk about nephrogenic diabetes insipidus.” Oh yes, we did.

    00:22 We did that in nephrology.

    00:23 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.

    00:36 And so, therefore, you will also will have polyuria and polydipsia.

    00:42 But, in that case, you would then have ADH levels being quite high because their receptors are resistant.

    00:51 Here we have SIADH.

    00:53 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 pituitary.

    01:11 Keep that in mind.

    01:13 Or there might be drugs such as Carbamazepine in which it may then result in increased release of ADH or you could be paraneoplastic.

    01:24 For example, a lung cancer that you should know of known as small cell lung cancer, huh, may result in increased release of ADH.

    01:34 Welcome to syndrome of inappropriate anti-diuretic hormone.

    01:38 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.

    01:48 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 high.

    01:57 You’re going to be forming concentrated urine, aren’t you? Now, what’s also important is the following.

    02:04 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.

    02:18 Remember, transudate to you should mean edema.

    02:20 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.

    02:30 Transudate, fluid in the interstitium, is there sodium in transudate? Yes or no? Yes, yes, yes.

    02:42 What is decrease in transudate is? Protein.

    02:47 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.

    02:59 So, an important distinction point is the following.

    03:03 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 significant? 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.

    03:27 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.

    03:44 That’s something important for you to figure out because if you’re thinking transudate...

    03:48 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.

    03:59 Here, you won’t find that.

    04:01 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.

    04:09 Symptoms - severe hyponatremia thus lethargic, seizures and coma.

    04:15 Now, hyper or hyponatremia, you will have CNS issues.

    04:21 Usually seen with acute reductions in serum sodium.

    04:28 Seen as disorders with SIADH.

    04:30 Causes.

    04:31 Now, keep in mind, trauma, we saw both with diabetes… central diabetes insipidus and SAIDH.

    04:42 Comes back to that point, if you destroy that posterior pituitary, there’s every possibility that here, you might be releasing too much ADH.

    04:49 And in the end, you might completely deplete your posterior pituitary resulting in what, please? Good, central diabetes insipidus.

    04:58 If you are unfamiliar with that spectrum prior, make sure that it is perfectly clear now.

    05:04 With that said, take a look – stroke, trauma, haemorrhage, infection, psychosis.

    05:10 What phase? The second phase.

    05:12 The first and second phase are the triphasic event during that neurosurgery.

    05:16 I’m not going to go through this one more time, I’ve talked about this plenty.

    05:21 Thoracic disease, this is a big one.

    05:24 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.

    05:38 Present with what? Plasma osmolality elevated, concentrated urine.

    05:43 Pneumonia, HIV patients with pneumocystis… bacterial, viral, TB; pneumonia may often present with SIADH.

    05:52 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.

    06:06 There are theories out there, but for the most part, you remember even the lung with cancer with small cell may result with SIADH.

    06:13 So, different things in the thoracic region often associated with SIADH.

    06:20 Drugs result in SIADH.

    06:23 SSRIs, chlorpromazine, carbamezapine, high-dose IV cyclophosphamide.

    06:31 It’s a list that you want to make sure that you memorize before taking your boards.

    06:37 Other causes of SIADH.

    06:42 Hereditary gain of function mutation.

    06:45 Alright, so, we’ll take a look at this.

    06:47 Here, it behaves like SIADH.

    06:50 You can have loss of function or gain of function.

    06:54 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.

    07:06 Where are these receptors located? Good, kidney.

    07:12 If it’s loss of function of the receptors, what’s your diagnosis? Nephrogenic diabetes insipidus.

    07:21 If it’s gain of function, it behaves like SIADH; urine here is going to be concentrated.

    07:30 These are type of questions that you’re going to get on your boards, absolute thinking questions.

    07:37 How common is this? Not very common, but what, do the boards love this? Oh yeah, they do because it’s asking you about gain and loss of function, completely changing your presentation and diagnosis of your patient.

    07:50 Here’s ectopic ADH, where? Thoracic.

    07:57 What cancer? Lung.

    07:59 What kind? Small cell lung cancer, a type of bronchogenic lung cancer.


    About the Lecture

    The lecture SIADH: Clinical Presentation by Carlo Raj, MD is from the course Pituitary Gland Disorders.


    Included Quiz Questions

    1. Presents with severely dilute urine
    2. Often asymptomatic
    3. Presents with associated hyponatremia
    4. Can be cause by carbamazepine
    5. Can be a result of a paraneoplastic syndrome
    1. It does not pit and is a transudate with little to no sodium present
    2. It consists of high protein exudate
    3. It can present with severe pitting and fluid stasis
    4. It is a hypernatremic transudate
    5. It will only be present in patients with heart failure
    1. Sheehan's syndrome
    2. CVA
    3. Trauma
    4. Infection
    5. Hemorrhage
    1. Doxycycline
    2. SSRIs
    3. IV cyclophosphamide
    4. Oxcarbezapine
    5. Chlorpropramide
    1. SIADH is gain of function of AVPV2 receptors, nephrogenic diabetes insipidus is loss of function
    2. SIADH is loss of function of AVPV2 receptors, nephrogenic diabetes insipidus is gain of function
    3. SIADH effects primarily AVPV2, nephrogenic diabetes insipidus effects primarily AVPV1
    4. Nephrogenic diabetes insipidus involves ectopic production of ADH, SIADH is gain of function of AVPV2
    5. Nephrogenic diabetes insipidus involves ectopic production of ADH, SIADH is loss of function of AVPV2

    Author of lecture SIADH: Clinical Presentation

     Carlo Raj, MD

    Carlo Raj, MD


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