Collecting Duct (CD): Summary of Clinical Findings

by Carlo Raj, MD

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    00:00 Now the three mechanisms or three plausible mechanisms as to why this is plausible. So this slide is then explaining to you. Take a look at the words or sentence in bold here.

    00:13 Three plausible explanations for the absence of pitting edema. Have I place enough emphasis on the fact that may be that you are not going to find pitting edema in your patient. I hope so. This is called aldosterone escape. You are paying attention to this graph that I just went through and it's a fact that in the middle there in experiment that is mimicking Conn in which your blood pressure no doubt is going to be elevated even though you are getting rid of your sodium, it diureses. This ladies and gentlemen is called aldosterone escape. You see that. Returning excretion of sodium to level of intake. Here once more what then happens to your effective arterial blood volume or you reabsorbed your sodium, increased effect of arterial blood volume? Next question pays attention. What happens to your hydrostatic pressure in the peritubular capillary? What happens to hydrostatic pressure in peritubular capillary when you have increased in effective arterial blood volume? Increased hydrostatic pressure in the peritubular capillary. So now it's resisting reabsorption. What happens to filtration fraction? Good. It decreases. Are we good here?. Lets continue. The three plausible of effects or explanations for the absence of the pitting edema, pressure natriuresis and with the whole thing results in sodium in the urine from inhibition of proximal reabsorption, why? Because of decrease in filtration fraction. Hence, I spent so much time attempting to explain to you how important it is for you to know that increase in hydrostatic pressure of the peritubular capillaries is going to then inhibit reabsorption resulting in a decrease in filtration fraction. Next, there could be an increase in ANP. How is that occurring? Increase in volume, sure with Conn's syndrome. Next, we are going to dilate the atria, sure you will and what are you going to release. Called atrial natriuretic peptide. A possible plausible explanation. Is it relevant for you? Yes it is, because you need to know ANP big time and that ANP will do everything in it's power to do what? Atrial natriuretic factor. What's natri means? Sodium. Uretic means diuresis. Number 3. Decreased concentration of thiazide-sensitive sodium chloride cotransporter possibly. The two big ones are the first and second one. This is called aldosterone escape thus giving you a plausible explanation as to why you wouldn't have pitting edema. What is pitting edema by the way? What is that? Transudate or exudate? I am sorry. What did you say? Good. Transudate. Be confident.

    02:58 You are right. Good. That transudate is what pitting edema is, only. What does that mean in terms of protein? It is protein poor, but it is full of what? Sodium, isn't it? It is protein poor transudate is. You are absolutely right, but do not forget. It is full of sodium.

    03:18 So if you don't have sodium even accumulating in there, can't have. What does pitting mean? You put your thumb or whatever on the inflammation and you take off your finger and oh my goodness there is no thumbprint. Well, I like my thumbprint. That is not so much good for your patient, but anyhow can I be any more dramatic. That is pitting edema, isn't it? Let us continue.

    03:40 Medullary collecting duct, where are you? Way down the collecting duct were just about to do what? We are about to enter my minor, major calyx. We are about to enter collecting duct in and out. You go into the ureter. Divided into inner and outer so be it. Responsible for a little bit of sodium reabsorption. We talked about all this in terms of aldosterone.

    03:58 Let us now move on to water. It is a major set of free. Stop there. Free water. What does that mean to you? Remember the difference that we talked about and you have discussed what physiology and in terms of free and obligated water. Allow the name to speak to you. An obligated water is one in which the water has been attached to some type of sodium or solute. Okay. Where are you? But the obligated water this was the water that was coming in from the Loop of Henley and it was moving through the thick ascending limb. What then happen to the thick ascending limb? You wept the sodium-potassium-2 chloride away from the water and now lets just call it a mother and I am just going to be dramatic here, the mother and the baby and that you are ripping the baby away from the mother. Come back, come back.

    04:53 But no, it doesn't want to. The child is free now. So that water is completely free of any type of attachment. That is free water. This is the diluting segment. That free water continues through the distal convoluted tubule comes down the collecting duct and ADH has an opportunity if needed to then reabsorb the free water only. What do you know about antidiuretic hormone? It only reabsorbs water, but there is a huge exception in which the ADH can only work by removing that urea as well.

    05:29 Overall summary, I have talked about every single segment of the nephron from proximal through descending limb, through the loop, through the thick distal collecting duct.

    05:45 Aldosterone in great detail. We put in all the major drugs. I just wish to ask you a couple of things before we end our lecture series on this note. Bartter's syndrome. Alphabetical order. What are you hitting first? It behaves like a loop diuretic. It works in the sodium- potassium-2 chloride channel. It works to disturb the concentrating ability of the nephron.

    06:12 You have hypercalciuria. That you do not have in Gitelman. Bartter syndrome may have hyperprostaglandinemia.

    06:21 Increased prostaglandin, management indomethacin big time, potassium sparing drug such as spironolactone.

    06:28 Bartter. If you go to Gitelman, we are working on the thiazide sensitive, in fact, the gene sodium chloride, thiazide sensitive gene or receptor, and Gitelman syndrome much more common than Bartter and with Gitelman some of the biggest differences is with Gitelman you have an issue with diluting ability not so much concentrating ability. Correct.

    06:54 Next as far as calcium is concerned, you do not have hypercalciuria, with Gitelman you have hypocalciuria. So these are some major pathologies we talked about there and down by the collecting duct, we talked about Addion's and Conn's and dealing with aldosterone. Full picture ladies and gentleman of the nephron from beginning to end, the physio, the pathology, the management. You know this, you are solid.

    About the Lecture

    The lecture Collecting Duct (CD): Summary of Clinical Findings by Carlo Raj, MD is from the course Diseases of the Nephron.

    Included Quiz Questions

    1. Pitting edema
    2. Secondary Hypertension
    3. Metabolic alkalosis.
    4. Polyuria
    5. Muscle weakness
    1. Decreased plasma renin activity
    2. Hyponatremia
    3. Decreased urine volume
    4. Hypertonic urine
    5. Hyperkalemia
    1. Plasma renin activity
    2. Angiotensin
    3. Cholesterol
    4. Desmolase
    5. ACTH
    1. Zona glomerulosa of adrenal cortex
    2. Zona fasciculata of adrenal cortex
    3. Zona reticulate of adrenal cortex
    4. Juxtaglomerular apparatus
    5. Anterior pituitary
    1. Decreased filtration fraction
    2. Decreased effective arterial blood volume
    3. Increased reabsorption
    4. Decreased hydrostatic pressure in the peritubular capillaries
    5. Decreased hydrostatic pressure in the glomerular capillaries
    1. …urinary sodium excretion returns to match levels of intake
    2. …plasma renin activity acts via negative feedback to decrease aldosterone concentration
    3. …aldosterone potency decreases due to overproduction
    4. …aldosterone activity is decreased by introducing drugs such as spironolactone
    5. …aldosterone receptors become over-saturated and are removed from the membrane
    1. Vasopressin
    2. Angiotensin II
    3. Calcitriol
    4. Parathyroid hormone
    5. Aldosterone
    1. It is protein rich fluid
    2. It is not found in patients with Conn’s syndrome
    3. It is fluid in the extracellular compartment
    4. It is sodium rich fluid
    5. It is transudative fluid
    1. ANP
    2. ADH
    3. Renin
    4. Angiotensin II
    5. Aldosterone
    1. It occurs with decreased filtration fraction
    2. It is due to inhibition of distal sodium reabsorption in the kidney
    3. It is a plausible explanation for the pitting edema in a patient with Conn’s syndrome
    4. It is associated with decreased renal plasma flow
    5. It is caused by decreased hydrostatic pressure in the peritubular capillary

    Author of lecture Collecting Duct (CD): Summary of Clinical Findings

     Carlo Raj, MD

    Carlo Raj, MD

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