The lesson. So, this practice question, you should have also in your lecture companion notebook, it's about diabetes insipidus. And I'll remind you again, we just read the passage more briefly than we would read a verbal reasoning passage. We take a quick glance through, and here, if this is me, and I'm seeing this chart, and mine doesn't have the ABCD labels that yours does.

I'm probably not even gonna look at the chart, because I'm just gonna say, if they ask me to understand the chart, then I'll understand the chart. So I see diabetes insipidus is where we don't have enough ADH. In central DI, okay, we don't have enough ADH produced by the posterior pituitary. And in nephrogenic DI, we have a kidney that does not respond to ADH. We have psychogenic polydipsia where there's a lot of drinking.

And then we have four patients subjected to a water deprivation test, so I say to myself, I'll go back and look at this and figure it out if they ask me to, and they do. So, which of the following patients has central DI? So now, I click back, or you're gonna be flipping back if you're following along in your lecture companion notebook, and you're gonna see central DI.

This is where ADH is not produced by the brain. So, I look at my chart now. So we have a watered, this is urine osmolarity. So we have A and B that as soon as we start depriving them of water, their urine osmolarity increases. I would guess that this is the psychogenic polydipsia folks.

Because they're drinking a bunch of water, but as soon as you make them stop, now all of a sudden, their urine is not as watery. And we move on. Administer ADH. Well, one person when we administer ADH, their urine stops being so watery. That is probably the person I would think with central diabetes insipidus, person C, because all of a sudden, they weren't able to make ADH.

Now we just give it to them instead, and they respond. Versus D, where even though we give it to them, and they don't respond, that's probably nephrogenic diabetes insipidus, person D. Because we give it to them, but even still, their kidney's not responding. So I'm guessing C is central DI, D is nefergenic DI. So central DI, and there it is, C.

So, as soon as we gave them ADH, all of a sudden, they're able to conc their urine as not as watery as it was. And I've already answered the next question. So, which of the following patients has nephrogenic DI? That's gonna be person D. Even though we gave them ADH, they failed to respond to it.

And there is the answer. Okay, following synthesis, ADH shares a common site of storage with which of the following hormones. So, ADH posterior pituitary, looking from the other posterior pituitary friend, and that's oxytocin. And they would potentially, a great MCAT question would be, and has been in the past what type of, where are they synthesized, and what type of connection brings them from the hypothalamus to pituitary?

So, synthesize in the hypothalamus, and they're brought down in the axon and stored in the posterior pituitary. Okay, there's our answer there, C. In addition to retention of water, ADH has what additional direct action? So, if we actually haven't discussed any other actions of ADH, and guess what? This is a classic MCAT thing to do here.

This is asking students to take things that they know, take something that's core knowledge for the MCAT, and extrapolate that knowledge out to something they don't know, but would make good sense. So, we know ADH is released in response to what? Low blood volume, and what else? Increased plasma osmolarity.

So, its action is to increase blood pressure. And it does that by retention of water. That's all we know about it. So, what else would it do? Will it increase urination? No, blood pressure would drop there, and that definitely doesn't line up with retention water.

So, I'm getting rid of A automatically. B, Sodium retention in the Loop of Henle. Well yeah, that would cause and increase blood pressure. So that might seem to fit, although, we've talked about ADH, and what it does in the kidney, and it would just retain water. So, that sounds more like some other hormone that's more in line with aldosterone, so not the exact right location.

So, we'll hold out B, it's not quite perfect, but it's on the right tract. C, decreased heart contractility, know if the heart wasn't beating as strong, then we would have even lower blood pressure. D, constriction of vascular smooth muscle, so this is great. This causes increased blood pressure. It's, and actually, we didn't know, but it seems to line up with what we know.

And the B is making us uneasy because we've studied ADH and its effect on the kidney, and it just opens all these poring channels. So, D does what we expect ADH to do, and it's in line with what we've already know about it. And that's the correct answer, and you're free to read the explanation. Okay, question 5, Conn's syndrome, so primary hyperaldosteronism.

So, we're gonna automatically think what does aldosterone do? Sodium retention get rid of potassium and water follow sodium out. So, what would we expect to see? Hypertension, absolutely, as water follows the sodium out, that should happen. Hypotension no, skin hyperpigmentation, tachycardia, no, we know hypertension absolutely fits, and those are not something we've heard about.

Now, here, we're clearly not being asked to extrapolate on our knowledge, because we should do know that if water follows that sodium out, we're gonna have increased blood pressure. And sure enough, that's the answer, hypertension. That's what happens in hyperadlosteronism. Another question on Conn's syndrome also causes hypokalemia.

That makes perfect sense. What effect does this have on membrane excitability in producing and action potential? So, this is not something that we discussed or know, but the second question here, asking us to take what we know. And try and use that and build on it.

So, these are two very hard MCAT questions. So, we're thinking what effect does potassium have on producing an action potential? Well, here is our little graph here. We know that we hang it on at negative 70, cuz we're more permeable to potassium at negative 90 than the sodium up here at positive 35 to 65, whatever you choose.

And here at negative 70, we're permeable to potassium, and this is reflecting the inside of the cell. And we remember, thanks to the sodium potassium pump, we have three sodiums out for every two potassium in. So, we have a bunch of potassium on the inside, not much on the outside. A bunch of sodium on the outside, not much on the inside.

Well, for hypokalemic, the potassium will increase out here, and it will increase in here. And the increase, sorry it will decrease out there and decrease inside as well. But the decrease on the inside is gonna be much more prominent, right? Because that's where most of our potassium is, and now we're going back to that reasoning that we did before.

If the inside of the cell, we're basing off that, we know it's negative. What if we lose these positively charged potassiums? As we lose positively charged potassium from the inside of the cell, the inside of the cell is going to get even more negative. So, instead of being negative 70, maybe now we'll be at negative 80, or something like that.

Well, the threshold is unchanged. It's still negative 55, right? So from negative nine, we had this far to go. Now, from an even more negative value of the inside of the cell, cuz we've lost those positively charged potassiums. We have even further to go now to get to that threshold value that we set as negative 55.

So, in hypokalemia, we have further to go and that is going to decrease the excitability of a neuron, and it decrease its ability to produce an action potential. Then we click forward, and that's the answer and the explanation should be essentially what I just told you. And how potassium, specifically hypokalemia, affects membrane excitability.

This is the conclusion of Biology 2, and I'll see you again for Biology 3.