Arginine Vasopressin (AVP) Differential Diagnoses

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.

00:47 Next.

00:48 That’s a concept.

00:50 If there’s ADH, what you’re doing to free water? You’re reabsorbing it.

00:54 So, therefore, how much free water are you clearing? Negative.

01:00 SIADH.

01:02 Give me some reasons.

01:04 Neurosurgery, transsphenoidal.

01:06 You might be releasing too much ADH.

01:09 Maybe there’s lung disease.

01:10 What kind? Maybe pneumonia, maybe there’s thoracic surgery or maybe lung cancer such as small-cell.

01:18 Whatever the reason, increased serum ADH abundantly.

01:21 We know about plasma and urine and we know about flow rate and there’s your clearance of free water.

01:26 Then we have water drinking.

01:30 If you’re drinking water or let’s say that you have primary polydipsia and you’re drinking water too much, excessively.

01:36 Here, things are different, aren’t they? You’re going to inhibit the release of ADH – decreased.

01:42 Your plasma osmolarity will be low.

01:46 Urine osmolarity is going to be extremely... well, if you’re drinking plenty of water, it will be hypoosmotic.

01:54 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.

02:01 So, therefore, this will be positive.

02:07 Other differentials.

02:09 Central diabetes insipidus.

02:11 Give me some causes.

02:12 Trauma, triphasic.

02:15 Eventually during transsphenoidal surgery, you may result in complete ablation of ADH.

02:22 Or we talked about infiltrative such as Langerhans cell histiocytosis.

02:26 Here you have decreased ADH.

02:28 Tell me about your urine.

02:32 Hypoosmotic.

02:33 Tell me about plasma osmolarity.

02:35 It will be hypersmotic.

02:37 Flow rate will be high.

02:39 Clearance of free water, if ADH is not present, will be positive.

02:43 If it’s nephrogenic, just to make sure we’re clear here, receptors aren’t working properly.

02:50 Your urine will be diluted, hypoosmotic.

02:54 High flow rate.

02:55 Positive clearance of free water.

02:57 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.

03:10 Your ADH levels will be really high, but the receptors aren’t working properly.

03:15 Keep that in mind.

03:18 Let’s talk about hyponatremia and the different, different types of hyponatremia.

03:26 You can have hypovolemic, euvolemic, hypervolemic.

03:29 I want you to really pause here for a second.

03:34 Take a look at the entire picture of this algorithm.

03:37 My topic is hyponatremia.

03:40 If it’s hyponatremia, the patient has decreased plasma sodium.

03:47 But, you can have different amounts of volume and still result in hyponatremia.

03:54 What does that mean? You could be hypovolemic, hypervolemic or euvolemic hyponatremic.

04:02 Then this gives you important differentials.

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

04:10 Examples: vomiting and diarrhoea.

04:13 Here, the patient is hypovolemic and also hyponatremic.

04:19 Overall picture of this slide is hyponatremia.

04:22 Let’s talk about euvolemia.

04:26 You rule out adrenal, adrenal insufficiency and you rule out hypothyroidism then you have SIADH.

04:36 This patient is euvolemic.

04:37 So, even though there is going to be hyponatremia and increased amounts of fluid in your patient, we still call this patient euvolemic.

04:46 Is that important? Yes, clinically it is.

04:49 That’s why you’re paying attention to that point.

04:52 In hypervolemic, you have renal failure, you have congest-congestive heart failure or you have cirrhosis.

04:59 In all three instances, you’re going to accumulate volume – hypervolemia.

05:06 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 fluid with sodium.

05:17 Think about right-sided heart failure, think about cirrhosis with decreased albumin or nephrotic syndrome with decreased albumin.

05:28 These patients are hypervolemic, hyponatremia.

05:32 In this section, we’re looking at two hormones of the posterior pituitary.

05:37 One of the great detail about ADH, oxytocin, a much simpler hormone to deal with.

05:44 Oxytocin, wherever it functions, take look at the picture, we have the uterus and we have the myoepithelial cells of the breast.

05:51 Wherever it functions, either the uterus or the breast, we’re talking about positive feedback in which is responsible for contraction, contraction, contraction.

06:00 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.

06:10 Contraction.

06:11 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.

06:23 It’s synthetized where? Paraventricular nuclei of the hypothalamus.

06:29 In fact, both posterior pituitary hormones are synthetized in hypothalamus.

06:36 It is then bound to neurophysin, brought into the posterior pituitary.

06:39 It’s important in parturition, meaning to say stimulation of the uterus and then with breast feeding with milk feeding.

06:50 Oxytocin – both circumstances, positive feedback.

06:53 Uterine contraction promotes uterine stretch.

06:56 Remember though that oxytocin and prostaglandin work in tandem so that you’re able to properly deliver your child.

07:04 The breast, specifically, histology here is the myoepithelial cells, as you see in the image.

07:10 Oxytocin used intravenously to induce or reinforce the labour.

07:16 And we have a drug called Atosiban, oxytocin receptor antagonist, used as a tocolytic in preterm labour.

07:25 Keep that in mind, please.

07:26 With slowing down contractions as being a major, major concept with oxytocin.

07:34 Ultimately, ADH and oxytocin management summary is what we’re looking at.

07:40 From the posterior pituitary, we have oxytocin.

07:44 With oxytocin, we have it at being a agonist to induce labour–welcome to Pitocin treatment indications.

07:55 Treatment indications or oxytocin in which you’re trying to slow down contraction.

08:03 The term here tocolytic.

08:06 You’re trying to lys the contraction, tocolytic.

08:11 The drug here, once again, Atosiban.

08:14 You want to try to slow down preterm labour, big time.

08:19 Now, on the other side, we have vasopressin and ADH.

08:23 Maybe perhaps you want to have agonist action.

08:27 Welcome to... remember, arginine, desmopressin, central diabetes inspidus.

08:33 Think about that patient in which, upon administration of desmopressin, you would then find urine osmolarity to then increase.

08:42 Antagonist, you remember that patient with SIADH? Would you tell me the steps of management? Number one, restrict free water use or consumption.

08:55 Number two, you want to crack that sodium maybe perhaps by giving? Good, IV fluids.

09:02 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.

09:15 Maybe perhaps you want to block your V2 receptors.

09:16 Welcome to Conivaptan (IV administration), Tolvaptan (p.o. administration).

09:23 If your disease or your pathology still seems refractory, you want to start thinking about maybe injuring your V2 receptors on purpose.

09:33 Welcome to drugs such as demeclocycline or lithium.