Collecting Duct (CD): Conn's Syndrome

by Carlo Raj, MD

My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides CD Pathophysiology RenalPathology.pdf
    • PDF
      Download Lecture Overview
    Report mistake

    00:00 Conn's syndrome, the opposite of Addison's, really. What is Conn's? It is the primary tumor located at the adrenal cortex. Where? As it produces too much cortisol. Listen.

    00:15 If you produce too much cortisol, how could you call that Conn's? You cannot. So if you produce too much cortisol that automatically puts you into the category in disease of and this is how black and white it is of Cushing syndrome. This is Conn's syndrome. Therefore, all I have is too much. Look at the first statement. A benign adenoma of the zona glomerulosa.

    00:39 So, therefore, resulting in you tell me, sodium quickly come on come on come on. Good. Increased sodium. Give me lab. Increased greater than 145. Next, potassium too much aldosterone you are getting rid of it, hypokalemia, potassium less than 3.5. Tell me about pH. Increased.

    00:59 You are getting rid of your hydrogen. That is probably one that is a little tricky. So whenever you go through acidosis, just make sure that you walk through that for me okay. So remember, too much aldosterone you get rid of hydrogen. You know I agree with you there. That gets a little tricky, but with the sodium-potassium that should be reflex.

    01:15 So in Conn's syndrome, you can expect to see metabolic alkalosis. Increased excretion of potassium, hypokalemia. We talked about all this. Look at this. Resting membrane potential, one more time, RMP. Close your eyes. Work with me. Don't just look at the words here. Conceptualize.

    01:34 Your potassium has been lost, hypokalemia. Resting membrane potential, more negative or more positive, please? More negative. What do you call that? If it becomes more negative, you do not call that depolarization. Look at what it says. Hyperpolarization okay. So if it become more negative, who is? The resting membrane potential, you're aware, further away from threshold. Are we clear now? So, therefore what happens to your muscle? It's much more difficult to have a all or none type of effect. Therefore, you will have muscle fatigue. Increased hydrogen secretion with Conn's syndrome, metabolic alkalosis. Now you tell me with all that sodium that we have here in Conn's, what kind of hypertension? It is not primary. It is secondary. So would you think that Conn's syndrome is not common? Just the opposite. It is common. It behoove you to really know Conn's syndrome in great detail. It behoove you to know aldosterone in great detail. Hence, all the time that we have spent really laying down the foundation of aldo, Conn's here, excess sodium. Let me ask you this one. This one is neat. Watch this. You have increased effective arterial blood volume. Not again Dr. Raj. I am. I have to.

    02:55 Alright. So, lets do this. If too much effective arterial blood volume, what does that even mean to you? It is the plasma component right. So you have all this blood coming to the kidney afferent arteriole increased, increased, increased. Right now skip over the glomerulus for me.

    03:08 I want you to enter the efferent arteriole and then I want you to enter the peritubular capillary. What happens to the hydrostatic pressure in the peritubular capillary with all of these blood volume? It increases. So what happens to reabsorption? It decreases because you are offering resistance, right. So with increased effect of arterial blood volume, what happens to your filtration fraction? Good. It decreases. We talked about that earlier.

    03:31 If you are not clear about that, I have given you specific slides about effective arterial blood volume and one in which we had a decrease effective arterial blood volume. Examples, hypovolemia may be due to hemorrhage or may be due to congestive heart failure. Remember that and the opposite. I gave you examples clinically of increased effective arterial blood volume in the headline of one of the causes was mineralocorticoid excess. What is Conn's syndrome? Mineralocorticoid excess. Stroke volume increases systolic blood pressure.

    04:05 Peritubular capillary, there it just then explains the filtration fraction. If you have too much volume, don't you want to get rid of your sodium? Of course, enhancing clearance of your sodium prevents the proximal tubule for reabsorbing sodium. What then happens to your filtration fraction, please? Diminishes.

    04:28 RAAS, now pay attention here. This we haven’t talked yet but it is important. So this is primary hypoaldosteronism. Who controls or regulates your aldosterone? If you say ACTH, I am not going to come out and slap you. I am not, but you begin the process or the cascade begins with ACTH. Picture this alright, okay. Be serious. Focus. ACTH anterior pituitary, adrenocorticotrophic hormone comes in through the blood hits the adrenal cortex. I agree. Next rate limiting enzyme, desmolase fantastic adrenal cortex. Where am I? Glomerulosa. So granted you begin the cascade of your adrenal cortical hormones with ACTH. I will give you that. Who finishes the job? There you go. Renin, renin, renin. So, therefore, for aldosterone the key regulator in terms of feedback is going to be what is known as plasma renin activity. Please, this is what you want to know clinically. Everything else of course things could be technical, but I will tell you one to be technical and one to be clinical. I am asking you kindly to be clinical with me. So if you have too much aldosterone, you are going to shut down plasma renin activity because why? A benign tumor in the adrenal cortex is producing too much aldosterone without even the need and the help and assistance of your renin. That is important.

    06:01 Next, excess sodium enters smooth muscle, but what does it cause it to do? Then there might be increased arteriolar pressure or resistance. It opens up calcium channel? We have increase in TPR. What do we have? Increase in diastolic blood pressure and these are the pathophysiologic explanations as to why you have an increase in a systolic blood pressure with increase in volume and sodium and increased diastolic blood pressure because of increased total peripheral resistance of the arterioles. But all together here you have it, you cannot miss a question from all the way down from basic sciences all the way up to your patient and presentation.

    06:40 Summary, hypertension, polyuria, muscle weakness, hypernatremia, hypokalemia, metabolic alkalosis.

    06:50 We walked through all of this in great detail. Now in your head, as you go through each one of these because you as a resident medical student, what have you? You walk into rotation and you see these things and you were explaining to your attending or to even your patient or your colleagues, this is what is going on? They will push you onto their shoulders and parade you around in rotation. How good do you feel? Pretty nice. Decreased PRA. What is happening? Plasma renin activity with primary hypoaldosteronism. What if you find an increase in renin? What would you call that perhaps? Secondary hypoaldosteronism, correct. Give me an example. Decreased perfusion to the kidney. You will find this to be interesting. I want you to focus upon the graph. There are three parameters on the Y axis here. Three different phases mean arterial pressure, cumulative sodium balance, urinary sodium excretion. There is an important concept that medicine wants you to know okay really is and is called aldosterone escape. We know it occurs because this is how patients present. That is why I have to give this to you and occurs very common because I told you Conn is found to be common. On the X axis are days. So lets say right in the middle this is an experiment to give you an understanding of Conn. In the middle is aldosterone. You see that. In the middle is the aldosterone that has been given. Immediately take a look at the mean arterial pressure. Shooting up. That is which you are paying attention right now. Listen to what I am saying and I am going to walk you through this. What is interesting too is the fact the sodium actually is going to decrease, amazingly. So even if you have Conn's syndrome and you have an increase in aldosterone granted, overall your sodium in your body is going to increase. Thus, the blood pressure will remain elevated as long as aldosterone is present. However, the way that the kidney works is the fact that you have a phenomenon called aldosterone escape where for aldosterone over the next few days, take a look at the X axis. What then happens to urinary sodium? Take a look at the bottom phase here. The bottom phase, the third bottom on, the urinary sodium, it quickly increases and you diuresis your sodium. Is this clinically relevant? Oh yes. This is how your patient is going to present. May I ask you something? Would you most likely find pitting edema in Conn's syndrome? No, not necessarily. That is why this experiment was necessary so that you clearly understand as to why you will not find pitting edema in Conn's syndrome as you would with congestive heart failure and congestive heart failure that's it you have continues to death of the heart. It is going to be systolic dysfunction and every single time aldosterone removes removes removes removes the fluid it keeps going into the interstitium because it can't move forward. Are we clear? Especially with right sided. In Conn's syndrome, your heart is perfectly fine and Conn is the problem with aldosterone in the adrenal cortex.

    About the Lecture

    The lecture Collecting Duct (CD): Conn's Syndrome by Carlo Raj, MD is from the course Diseases of the Nephron.

    Included Quiz Questions

    1. Zona glomerulosa
    2. Kidney glomerulus
    3. Zona reticularis
    4. Zona fasciculata
    5. Anterior pituitary gland
    1. Elevated plasma volume, elevated sodium, decreased potassium, elevated blood pH.
    2. Elevated plasma volume, elevated sodium, elevated potassium, elevated blood pH.
    3. Decreased plasma volume, elevated sodium, decreased potassium, decreased blood pH.
    4. Decreased plasma volume, decreased sodium, decreased potassium, decreased blood pH.
    5. Elevated plasma volume, decreased sodium, elevated potassium, elevated blood pH.
    1. Increased systolic BP, increased diastolic BP, increased plasma volume, decreased plasma renin activity.
    2. Decreased systolic BP, decreased diastolic BP, decreased plasma volume, decreased plasma renin activity.
    3. Increased systolic BP, normal diastolic BP, increased filtration fraction, increased plasma renin activity.
    4. Increased systolic BP, normal diastolic BP, decreased filtration fraction, decreased plasma renin activity.
    5. Normal systolic BP, increased diastolic BP, normal filtration fraction, decreased plasma renin activity.
    1. In secondary hyperaldosteronism, plasma renin activity is increased.
    2. In primary hyperaldosteronism, plasma renin activity is increased.
    3. In primary hyperaldosteronism, the total peripheral resistance in arterioles is decreased.
    4. In secondary hyperaldosteronism, the effective arteriolar blood volume is decreased.
    5. In secondary hyperaldosteronism, the diastolic BP is decreased.
    1. Conn’s syndrome patients typically do not present with lower extremity pitting edema due to the ‘aldosterone escape’ phenomenon.
    2. Conn’s syndrome patients typically do not present with hypokalemia due to the ‘aldosterone escape’ phenomenon.
    3. Conn’s syndrome patients typically do not present with hypertension due to the ‘aldosterone escape’ phenomenon.
    4. Conn’s syndrome patients typically present with hyponatremia due to the ‘aldosterone escape’ phenomenon.
    5. Conn’s syndrome patient presentation is typically unaffected by the ‘aldosterone escape’ phenomenon as it is only observed in experimental conditions.

    Author of lecture Collecting Duct (CD): Conn's Syndrome

     Carlo Raj, MD

    Carlo Raj, MD

    Customer reviews

    5,0 of 5 stars
    5 Stars
    4 Stars
    3 Stars
    2 Stars
    1  Star