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Arginine Vasopressin (AVP) Differential Diagnoses

by Carlo Raj, MD
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    00:00 Let’s take a look at important arginine vasopressin differential diagnoses.

    00:04 Once you’ve understood all of different topics that we covered up above, you go to this table and you take a look at the labs so that you’re able to clearly and quickly differentiate one pathology from the other.

    00:17 And not all these are pathology.

    00:18 Some of these are pathophysiologic point.

    00:20 For example, water deprivation.

    00:22 Close your eyes.

    00:23 The water deprivation, what’s your plasma osmolarity? Increased.

    00:26 What’s your urine osmolarity? Increased.

    00:29 Water deprivation.

    00:31 Osmoreceptors of hypothalamus.

    00:32 You tell me.

    00:33 Stimulated, ADH comes out.

    00:36 Therefore, you can expect your serum ADH to be increased.

    00:40 First column.

    00:41 You tell me about plasma urine osmolality.

    00:44 Done.

    00:45 Flow rate – obviously, low because you’re reabsorbing water.

    00:49 Stop.

    00:50 Concept.

    00:51 Clearance means what? It doesn’t mean filtration, doesn’t mean reabsorption, it does not mean excretion.

    00:59 It means what you’ve actually cleared out of the body.

    01:02 Clearance, in other words, excretion.

    01:05 Of what? Free water.

    01:07 What does free water mean to you? It’s water that is not obligated to sodium.

    01:11 It’s not obligated water, it’s free water.

    01:13 Next.

    01:14 That’s a concept.

    01:16 If there’s ADH, what you’re doing to free water? You’re reabsorbing it.

    01:20 So, therefore, how much free water are you clearing? Negative.

    01:27 SIADH.

    01:28 Give me some reasons.

    01:30 Oh, the triphasic, first and second triphasic.

    01:34 Neurosurgery, transsphenoidal.

    01:37 You might be releasing too much ADH.

    01:39 Maybe there’s lung disease.

    01:41 What kind? Maybe pneumonia, maybe there’s thoracic surgery or maybe lung cancer such as small-cell.

    01:48 Whatever the reason, increased serum ADH abundantly.

    01:52 We know about plasma and urine and we know about flow rate and there’s your clearance of free water.

    01:57 Then we have water drinking.

    02:00 If you’re drinking water or let’s say that you have primary polydipsia and you’re drinking water too much, excessively.

    02:07 Here, things are different, aren’t they? You’re going to inhibit the release of ADH – decreased.

    02:13 Your plasma osmolarity will be low.

    02:17 Urine osmolarity is going to be extremely... well, if you’re drinking plenty of water, it will be hypoosmotic.

    02:24 The flow rate will be incredibly high and the amount of water that you’re now clearing, in terms of free water, will be excessive.

    02:32 So, therefore, this will be positive.

    02:38 Other differentials.

    02:39 Central diabetes insipidus.

    02:41 Give me some causes.

    02:43 Trauma, triphasic.

    02:45 Eventually during transsphenoidal surgery, you may result in complete ablation of ADH.

    02:52 Or we talked about infiltrative such as Langerhans cell histiocytosis.

    02:57 Here you have decreased ADH.

    02:59 Tell me about your urine.

    03:02 Hypoosmotic.

    03:04 Tell me about plasma osmolarity.

    03:05 It will be hypersmotic.

    03:07 Flow rate will be high.

    03:09 Clearance of free water, if ADH is not present, will be positive.

    03:14 If it’s nephrogenic, just to make sure we’re clear here, receptors aren’t working properly.

    03:21 Your urine will be diluted, hypoosmotic.

    03:24 High flow rate.

    03:26 Positive clearance of free water.

    03:28 If the receptor, for whatever reason, is not working maybe due to demeclocycline or lithium or the V2 receptors are congenitally not functioning, this is nephrogenic diabetes insipidus.

    03:41 Your ADH levels will be really high, but the receptors aren’t working properly.

    03:46 Keep that in mind.

    03:48 Let’s talk about hyponatremia and the different, different types of hyponatremia.

    03:57 You can have hypovolemic, euvolemic, hypervolemic.

    03:59 I want you to really pause here for a second.

    04:04 Take a look at the entire picture of this algorithm.

    04:08 My topic is hyponatremia.

    04:11 If it’s hyponatremia, the patient has decreased plasma sodium.

    04:18 But, you can have different amounts of volume and still result in hyponatremia.

    04:25 What does that mean? You could be hypovolemic, hypervolemic or euvolemic hyponatremic.

    04:33 Then this gives you important differentials.

    04:35 Let’s take a look at our first branch of the algorithm for hyponatremia and we have hypovolemia.

    04:41 Examples: vomiting and diarrhoea.

    04:44 You need to make sure that you rule out nephrotic syndrome.

    04:47 Here, the patient is hypovolemic and also hyponatremic.

    04:52 Overall picture of this slide is hyponatremia.

    04:56 Let’s talk about euvolemia.

    05:00 You rule out adrenal, adrenal insufficiency and you rule out hypothyroidism then you have SIADH.

    05:10 This patient is euvolemic.

    05:11 So, even though there is going to be hyponatremia and increased amounts of fluid in your patient, we still call this patient euvolemic.

    05:20 Is that important? Yes, clinically it is.

    05:23 That’s why you’re paying attention to that point.

    05:26 In hypervolemic, you have renal failure, you have congest-congestive heart failure or you have cirrhosis.

    05:33 In all three instances, you’re going to accumulate volume – hypervolemia.

    05:40 In all three instances with renal failure, we can talk about this as being nephrotic syndrome perhaps or renal failure itself, in which you are then retaining transudate or fluid with sodium.

    05:54 Think about right-sided heart failure, think about cirrhosis with decreased albumin or nephrotic syndrome with decreased albumin.

    06:04 These patients are hypervolemic, hyponatremia.

    06:07 I want to show you a graph here and show you how to dissect your graphs from physio, but then apply it in terms of what’s going on here in pathology.

    06:20 When the X-axis is urine flow rate, always, always dissect your graph with the following parameters.

    06:29 The Y-axis represents your urine plasma osmolarity.

    06:33 You’ll notice, as you go from X to Y, that the urine flow rate from left to right is increasing.

    06:44 As you go from X to Y, your urine and plasma osmolarity is decreasing.

    06:52 You should already be predicting as to what kind of patient is this.

    06:58 Is this a patient who is having issues with ADH? Is this a patient who’s having issues with the kidney? Let’s say that you’re drinking water.

    07:09 If you’re drinking water, what can you expect your plasma osmolarity to do? Decrease.

    07:16 Where are you on this graph? The Y-axis.

    07:19 You’re decreasing.

    07:23 If you’re drinking water, what should happen to ADH release? Are you going to stimulate the osmoreceptors and therefore, triggering the release of ADH or are you inhibiting the osmoreceptors, therefore inhibiting the release of ADH? If all you’re drinking is... all you’re doing is drinking water, you’re causing your plasma osmolarity to decrease.

    07:49 You’re going to inhibit the release of ADH.

    07:51 Therefore, a type of urine that you’re producing is diluted urine.

    07:58 You, at this point, should be able to predict that the patient does not have a kidney issue.

    08:05 In fact, this is a perfect normal patient that is being doing what? Drinking water.

    08:11 Once you’ve understood the concept, all you’re doing is looking for the answer.

    08:19 Is it A, oral ingestion of 1L water? Is it oral ingestion of 200 mL of normal saline or ingestion of 200 mL of hypertonic glucose solution? Is it oral ingestion of 200 mL of 3% saline or injection of ADH? The ones that you can rule out quickly, for sure E as in epsilon, because if you injected ADH, what kind of patient? Normal patient.

    08:48 You definitely wouldn’t expect the urine osmolarity to decrease, would you? Take out E.

    08:53 Now you’re left with A through D. Let’s take a look at the normal saline.

    08:59 If you have normal saline that you’re giving your patient, then you can expect this to be isotonic, isotonic.

    09:06 Therefore, you’re not going to have any change.

    09:09 Remember, this takes you back to physiology with the [Inaudible 00:09:11].

    09:15 And you should remember and accept that if you are ingesting isotonic fluid, all that you’re doing is increasing your [Inaudible 00:09:23] volume without changing the tonicity.

    09:27 You can rule out B.

    09:28 So, B and E has been ruled out.

    09:30 Now, you’re left with hypertonic and hypertonic.

    09:35 C and D. Look, what’s normal saline? 0.9%.

    09:41 3% saline is hypertonic.

    09:43 I mean, ridiculously hypertonic.

    09:46 And then hypertonic glucose solution.

    09:48 What is that going to do to your plasma osmolarity? Predict.

    09:53 Should increase it.

    09:54 What’s happening to my patient on the graph? Plasma osmolarity is decreasing.

    09:59 How in the world could it be C, as in Charlie, or D, as in delta? It cannot.

    10:04 You’re left with A, as in alpha.

    10:07 In this section, we’re looking at two hormones of the posterior pituitary.

    10:11 One of the great detail about ADH, oxytocin, a much simpler hormone to deal with.

    10:18 Oxytocin, wherever it functions, take look at the picture, we have the uterus and we have the myoepithelial cells of the breast.

    10:26 Wherever it functions, either the uterus or the breast, we’re talking about positive feedback in which is responsible for contraction, contraction, contraction.

    10:34 A simple question that you want to keep in mind would be, well, if it’s contraction, then what is the G protein that you’re referring to? Gq, right? Gq.

    10:45 Contraction.

    10:46 Oxytocin responsible for contraction of uterus so that you deliver the child and then also during suckling by an infant, with the mother you’re going to then eject milk.

    10:58 It’s synthetized where? Paraventricular nuclei of the hypothalamus.

    11:03 In fact, both posterior pituitary hormones are synthetized in hypothalamus.

    11:10 It is then bound to neurophysin, brought into the posterior pituitary.

    11:14 It’s important in parturition, meaning to say stimulation of the uterus and then with breast feeding with milk feeding.

    11:25 Oxytocin – both circumstances, positive feedback.

    11:28 Uterine contraction promotes uterine stretch.

    11:31 Remember though that oxytocin and prostaglandin work in tandem so that you’re able to properly deliver your child.

    11:39 The breast, specifically, histology here is the myoepithelial cells, as you see in the image.

    11:45 Oxytocin used intravenously to induce or reinforce the labour.

    11:50 And we have a drug called Atosiban, oxytocin receptor antagonist, used as a tocolytic in preterm labour.

    12:00 Keep that in mind, please.

    12:01 With slowing down contractions as being a major, major concept with oxytocin.

    12:08 Ultimately, ADH and oxytocin management summary is what we’re looking at.

    12:15 From the posterior pituitary, we have oxytocin.

    12:19 With oxytocin, we have it at being a agonist to induce labour... welcome to Plocin treatment indications.

    12:32 Or oxytocin in which you’re trying to slow down contraction.

    12:37 The term here tocolytic.

    12:38 You’re trying to lys the contraction, tocolytic.

    12:45 The drug here, once again, Atosiban.

    12:47 You want to try to slow down preterm labour, big time.

    12:53 Now, on the other side, we have vasopressin and ADH.

    12:58 Maybe perhaps you want to have agonist action.

    13:01 Welcome to... remember, arginine, desmopressin, central diabetes inspidus.

    13:08 Think about that patient in which, upon administration of desmopressin, you would then find urine osmolarity to then increase.

    13:16 Antagonist, you remember that patient with SIADH? Would you tell me the steps of management? Number one, restrict free water use or consumption.

    13:27 Number two, you want to crack that sodium maybe perhaps by giving? Good, IV fluids.

    13:36 Next, you want to try to get rid of the excess fluid, so you give a loop diuretic, but once again, make sure that you keep an eye on that sodium because your patient is severely in a state of hyponatremia.

    13:49 Maybe perhaps you want to block your V2 receptors.

    13:51 Welcome to Conivaptan (IV administration), Tolvaptan (p.o. administration).

    13:57 If your disease or your pathology still seems refractory, you want to start thinking about maybe injuring your V2 receptors on purpose.

    14:08 Welcome to drugs such as demeclocycline or lithium.


    About the Lecture

    The lecture Arginine Vasopressin (AVP) Differential Diagnoses by Carlo Raj, MD is from the course Pituitary Gland Disorders.


    Included Quiz Questions

    1. Nephrogenic diabetes insipidus
    2. SIADH
    3. Central diabetes insipidus
    4. High water intake
    5. Water deprivation
    1. Nephrotic syndrome
    2. SIADH
    3. Addison's disease
    4. Hypothyroidism
    5. Paraneoplastic syndrome
    1. Urine osmolarity decreases
    2. Urine osmolarity increases
    3. Clearance of water decreases
    4. Plasma osmolarity increases
    5. Plasma osmolarity decreases
    1. Results in increased cAMP in target cells
    2. Synthesized in paraventricular nuclei of the hypothalamus
    3. Stored in posterior pituitary
    4. Stimulates Gq receptors
    5. Induces a positive feedback response
    1. Tocolytic and oxytocin receptor antagonist
    2. Synthetic form of oxytocin
    3. Promoter of breast myoepithelial contractions to promote lactation
    4. Enhance positive feedback loop initiated by oxytocin
    5. Enhance uterine contractions to promote labor

    Author of lecture Arginine Vasopressin (AVP) Differential Diagnoses

     Carlo Raj, MD

    Carlo Raj, MD


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