Thiazide Puns

If these drugs are meant to cause diuresis via excreting sodium which follows water, why is it that in the collecting duct, sodium is re absorbed into blood, which again follows water. I'm trying to study this but it's paradoxical. What am I missing?

Both of those diuretics act on transporters that ultimately results in reduced reabsorption of chloride—at least locally. If so, then why only loop thiazides lead to hypochloremia?

Thank you.

I go to school for pharmacology and my midterm is wednesday </3

below is what it says in my study material (which I can't wrap my head around)

https://preview.redd.it/jbrinn3sj7181.png?width=746&format=png&auto=webp&s=f929c7d97f13ba8fe2afd90470460b2d4ab1a321

Thank you for reading this.

Cystic medullary kidney disease:

• Umod reduction -> reduced apical expression of NKCC transporter in thick ascending loop of Henle -> volume contraction -> RAAS activation -> sodium reabsorption. Uric acid reabsorption then follows sodium reabsorption -> hyperuricemia

Loop diuretics:

• Functionally same mechanism as above.

Thiazide diuretics:

• Hyperuricemia from RAAS compensation due to natriuresis

ENaC and aldosterone inhibitors:

• We still see angiotensin II elevation, which would lead to increased PCT sodium reabsorption. Yet, we don't see hyperuricemia.

Mannitol:

• RAAS activation is intact. Yet, we don't see hyperuricemia.

Do we know what that is?

Thank you.

.

How do thiazide diuretics increase serum lithium levels? And how do K sparing diuretics decrease li levels?

I'm specifically wondering how bemetizide (+triamterene) compares to chlortalidone and hydrochlorothiazide (+triamteren).

I already know that the half lives of bemetizide and hydrochlorothiazide are relatively similar, while the half life of chlortalidone is way longer. (also obviously chlortalidone isn't combined with a potassium-sparing diuretic)

Can anyone explain why nephrogenic diabetes insipidus is treated with thiazide diuretics?

Thiazide diuretics decreases Na reabsortion. So, water reabsorption will be decreased too, since it follows Na. But isn't the goal to increase water reabsorption in diabetes insipidus?

Can someone explain to me the mechanism of action of how thiazides are used to treat nephrogenic diabetes insipidus? thanks!

I've found sources that say it's a function of more Na+ and water reaching the collecting duct, but what exactly is the mechanism? Thanks!

Seems counterintuitive to give a diabetic person a diuretic

Why doesn’t it worsen it? Thanks in advance..

*Thiazide diuretic QID 18553 in UW. Can someone explain?

Hello everyone!

So I'm having trouble with a certain concept:

How do thiazides work?

My understanding is that by blocking NaCl channels in the DCT, they will get rid of Na+ and water will follow Na+ out. Is this correct reasoning?

What does Ca have to do with thiazides then? Where does the Calcium part come from?

Also, why are they used to treat nephrogenic diabetes insipidus? What's the mechanism behind that?

If anyone can give some insight into this I would really appreciate it! Thanks in advance!!

Hi everyone, tried to search for an answer on here but couldnt find one. According to sketchy, loop and thiazide diuretics cause hypokalemia due to increased delivery of sodium to the collecting duct. that increased sodium in the collecting duct is reabsorbed through ENacs and that then leads to potassium excretion (due to negative intraluminal concentration?). i think get that but when i think about how "water follows sodium" i get confused. if the sodium is being reabsorbed through those ENacs why are the diuretics still working? wouldnt the water you just tried getting rid of with diuretics get reabsorbed back? not sure if what i wrote makes sense but thanks for any help anyone can give

Can someone explain how these diuretics cause metabolic alkalosis?

I'm not sure why it causes contraction alkalosis. Thanks!

According to Sketchy, calcium reabsorption is mediated by thiazide-induced activation of the basolateral NCX, but what about magnesium? What causes it to be wasted? Thank you all so much!

I understand that there is activation of RAAS with Bartter's and Gitelman's, but there's also RAAS activation with the K-wasting diuretics as well. :( Please end a poor sleep-deprived student's misery!

How does Hydrochlorothiazide change Ca levels?

Okay ladies and gentlemen, we all have been highly agitated by NBME 20's thiazide=galactorrhea question. It's nowhere mentioned in FA, it's no where online, it's not in uworld, it's not in Katzung/Trevor, and it's not even on uptodate.

HOWEVER, when the USMLE question writers said that they want us to understand concepts, THEY REALLY MEANT THAT.

I stumbled upon this epiphany after banging my head against endo/renal, just by luck was reading them together on the same day in FA.

It turns out, thiazides decrease GFR. This should be a no brainer. HOWEVER, prolactin *EXCRETION* is done partly by the kidneys.

This drop in GFR leads to elevated levels of prolactin, resulting in galactorrhea.

To confirm this, I typed in "kidney failure" and "prolactin" --> https://www.ncbi.nlm.nih.gov/pubmed/26299069 - 2015 study. The only way to have gotten this question right was to really have a deep understanding of the kidneys, renal drugs, and the appropriate physiology.

TL;DR

Thiazide --> decrease GFR --> Elevated prolactin --> galactorrhea

Hello!

Hope this message finds you all well. Was having a discussion today regarding the administration of HCTZ with furosemide. My team was relaying that some had heard that HCTZ should be given 30 minutes before, whereas another stated it should be a few hours. I've looked up the original trials on combined therapy, and none seem to mention timing. I was curious if any of you had more information on best practice, and/or any supportive literature. Thanks!

I’m learning about meds for DVT and PVD along with meds. I’m a bit confused on when and why you’d use one or the other for a patient. I know thiazide causes calcium retention and loops enhance calcium loss but for some reason I can’t wrap my head around why one would be used vs the other. Sorry if it’s a dumb question. Thank you!

Can someone explain to me why thiazide diuretics are the first pharmacological treatment for hypertension over loop diuretics? I’m trying to understand the differences between the two.

Honestly, I don't understand the mechanism behind this

Can someone explain the mechanism why thiazides causes hyponatremia and why furosemide cause excessive diuresis ?