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SIADH: Clinical Presentation

by Carlo Raj, MD
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    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 diabetes insipidus.” 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 are resistant. 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 pituitary. 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 hormone. 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 high. 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...

    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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