Tubuloglomerular Feedback

00:00 Now, that tubuloglomerular feedback that I was referring to, stop there for one second and dissect the name. Tubulo, what does that represent? It represents the urine.

00:12 The glomerulus, what does that represent? The glomerulus. So they are going to what? They're going to communicate with one another. How is that possible? The afferent arteriole has the juxtaglomerular cells, the apparatus. Go back and take a look at that picture.

00:28 Which picture? The one with JG cells and the macula densa. The macula densa is going to sense what? It will sense the chloride or maybe the sodium in your urine. Whatever. It doesn’t matter.

00:38 Sodium and chloride are buddies. They’re always moving together. One is a cation. One is an anion.

00:43 They’re magnetically stuck together, right? Okay. So now, what’s my issue? What may then happen with tubuloglomerular feedback is that if you were to give your patient a loop diuretic, why? Maybe there’s high blood pressure, maybe your patient has pulmonary edema secondary to left-sided heart failure and you needed to then relieve dyspnea. Are we clear? Is that a good time to perhaps use a loop diuretic to reduce the pulmonary edema? Yes, it is.

01:09 So by giving this, what do you expect to do? You expect there to be massive diuresis.

01:15 Where does the loop diuretic work? In pharmacology, what did you learn? It knocks out the sodium potassium two chloride, doesn’t it? Yes, it does. Now, that’s in pharm.

01:24 As we progress further, we’re going to get into some pathology. So now, with a loop diuretic, that TGF is completely blunted. So therefore, that feedback between the two, meaning the tubules, macula densa and the afferent arteriole, is not going to happen anymore. And so therefore, you’re going to continue diuresing. Next, what else? In pathology, let’s say that you have renal artery stenosis. Okay, that patient again: 53-year-old male, hypertension, 160 over 90, what kind? Secondary hypertension. The renal artery stenosis was caused by atherosclerosis.

02:03 So far, so good. And if that decreased perfusion was to continue, then, oh, oh, who’s going to be damaged? The tubule. What is it called? Acute tubular necrosis.

02:18 So acute tubular necrosis is when you have ischemia being one of the most common causes of ATN.

02:23 In fact, you could have drugs as well. But let’s just go with the most common.

02:27 Ischemia resulting in A-acute, T-tubular, N-necrosis. Guess how well my tubules are working.

02:37 It’s not. So once again, you get blunting of your tubuloglomerular feedback. Not good.

02:43 The tubules aren’t working properly. And we can confirm that later on when we start doing our issues with what’s called azotemia. You've heard of that, right? We’re going to further detail.

02:55 If you’re not clear about azotemia, trust me, you will be by the time we’re done.