Collecting Duct (CD): Different Channels in Different Ducts

00:00 Next, all these are things that we have talked about over and over again. Here is everything officially for you in words. Aldosterone, reabsorption of sodium, excretion of potassium, sodium diffuses into the cell, the primary site here where potassium is to get rid of it for aldosterone. Sodium-potassium pump. Know its activity with aldosterone. It reabsorbs the sodium. It gets rid of the potassium. Ultimately if you have too much aldosterone, it may result in hydrogen getting rid of and may result in getting rid of your potassium hypokalemia. The bicarb is reabsorbed into the ECF causing metabolic alkalosis. So remember whenever there is issues with hydrogen, you are getting rid of it as soon as you think about hydrogen and bicarb, you are thinking about that formula and for the most part, there even though it is not pictured, I assume that you know at this juncture with hydrogen and bicarb, they are going to be all part of the carbonic anhydrase formula, aren't they? And what kind of direction are they always moving in with bicarb and hydrogen? In opposite direction. So wherever were hydrogen is going, let it be into the lumen or into the blood, bicarb will be moving in the opposite direction. Here hydrogen will be moving into the urine with the help of aldosterone and then your bicarb will be coming out into the blood all contributing to your metabolic alkalosis. Now, a couple of important potassium-sparing drugs, that you want to keep in mind especially for example let me give you a clinical situation.

01:42 If you have a patient who has hypokalemia secondary to loop diuretics, correct. And so therefore, you might want to think about giving that patient a potassium sparing drug. With amiloride and triamterene, little bit different, isn't it? Because these are not drugs that work on the aldosterone receptor. These are drugs that work on the luminal. Highlight that in your head. Membrane sodium channel. Inhibits sodium reabsorption and thus inhibits potassium excretion. Isn't that the point of these drugs is to spare the excretion of potassium, isn't it? The effect of increased distal delivery of sodium, pay attention, loop or thiazide, the increased delivery of sodium because you are blocking the sodium channels of different types. Loop where are you? The case in England. Thiazide, where are you? DCT while the diuretics acting proximal to this channel, augmented sodium reabsorption and potassium excretion, may produce hypokalemia if potassium supplements are not taken. So often times when this is going to be increased delivery of sodium, please understand that sodium is going to try to be reabsorbed and potassium potentially could be lost. Hypokalemia may produce metabolic alkalosis. So you can think of this as being a natural form of aldosterone and this is a problem when you give such diuretics that end up increasing delivery of sodium. So, effective increase distal delivery of sodium from loop and thiazide diuretics acting proximal to this channel. What channel? Proximal to collecting duct and if you increase the delivery of sodium to it and whatever the cause maybe keep this in mind that it behaves like a natural aldosterone. It will do everything in it is power to reabsorb the sodium, gets rid of potassium and gets rid of hydrogen. Do not forget that, please. That is an important point clinically.