Great question - they lead to mild hypovolemia which activates the RAAS which leads to enhanced sodium and water reabsorption in the PCT which leads to less polyuria. Although it seems paradoxical it does seem to be effective in nephrogenic DI
@NinjaNerdOfficial I had this exact same question too and loved your explanation of it here as well. I have a follow up question to add on to it if that's okay. If the cause of the nephrogenic DI is hypokalemia or hypercalcemia, then I assume you correct the abnormality (and/or underlying cause) and you solve the issue. But in instances of CKD or inheritance, do you keep them on long term thiazide tx? Lifetime?
In complications of SIADH: The increase in aquaporin channels increases re-uptake of water from the urine, which leads to dilution of blood, and thereby, hyponatremia. But the increased water retention would lead to decreased aldosterone (to counteract the hypervolemia), which would promote sodium excretion in the urine. Water follows sodium, so more water should go into the urine, but since ADH is increased, it just refuses to let that water go, and continues the pattern. How then, would euvolemia be achieved? @ euvolemic hyponatremia
Salt tablets have no effect in treatment at all, every nephrologist will get a heart attack if you administer them to your patients. Fluid restriction is key to recompensate the normal state of sodium levels in chronic and/or asymptomatic patients if the Na is between 120-135 mmol/l. If acute or symptomatic the i.v. treatment is the way to go but as slowly as possible, max 10 mmol/l per day. Otherwise you risk an irreversible central pontine myelinolysis.
I was worried you might be gone from this channel forever. But I kept the faith. Welcome back, man. 🙏
ur carrying my entire MD on ur gd back... my tuition should go to u, my guy
I love the diagnostic algorithm part at the end. It really helps with consolidating the information. 🙌
Beautifully explained with crystal clear concepts , Thank you so much sir 😊, your videos are very informative and helpful to us ..😊
Incredible the best way of teaching ❤❤❤ but please come to the whiteboard bcz we love your diagnostic explanation 😊
I want to shake your hand in person after getting this Medical degree!
Thank you for your video. I learned a lot even though, I'm student nurse.
If u teach like that am not able to understand
Love from India 🇮🇳🇮🇳
Great video, thanks Ninja Nerd!
Please teach diagnostic approaches on board
Thank you so much! you made this topic so easy and understandable!!! THE BEST!!!
Why are Thiazide diuretics used for treating nephrogenic DI although they promote diuresis...?🤔
Great question - they lead to mild hypovolemia which activates the RAAS which leads to enhanced sodium and water reabsorption in the PCT which leads to less polyuria. Although it seems paradoxical it does seem to be effective in nephrogenic DI
@@NinjaNerdOfficial Thanks boss...🙏
@NinjaNerdOfficial I had this exact same question too and loved your explanation of it here as well. I have a follow up question to add on to it if that's okay. If the cause of the nephrogenic DI is hypokalemia or hypercalcemia, then I assume you correct the abnormality (and/or underlying cause) and you solve the issue. But in instances of CKD or inheritance, do you keep them on long term thiazide tx? Lifetime?
INCREDIBLE TEACHER!
Love this guy so much ❤️❤️❤️❤️❤️🤌🏼🤌🏼🤌🏼🤌🏼🤌🏼🤌🏼
Thank you alot for this effort ❤
Sir. You're my hero
great video as always, thank you very much!
I st like sir, I'm pratheesh from india( tamilnadu).big fan of you sir.say one hii sir.
hi
Plz do make videos on solving uworld
In complications of SIADH: The increase in aquaporin channels increases re-uptake of water from the urine, which leads to dilution of blood, and thereby, hyponatremia. But the increased water retention would lead to decreased aldosterone (to counteract the hypervolemia), which would promote sodium excretion in the urine. Water follows sodium, so more water should go into the urine, but since ADH is increased, it just refuses to let that water go, and continues the pattern. How then, would euvolemia be achieved? @ euvolemic hyponatremia
Great video
BMP= Basic Metabolic Panel
His biceps🔥
Thank you so much ☺️
Thank you so mutch
SIADH causes peripheral edema and high blood pressure?
Salt tablets have no effect in treatment at all, every nephrologist will get a heart attack if you administer them to your patients. Fluid restriction is key to recompensate the normal state of sodium levels in chronic and/or asymptomatic patients if the Na is between 120-135 mmol/l. If acute or symptomatic the i.v. treatment is the way to go but as slowly as possible, max 10 mmol/l per day. Otherwise you risk an irreversible central pontine myelinolysis.
Tnx
Can't we tell the difference of Diabetes Insipidus versus Psychogenic Polydipsia by looking at just serum osmolarity and urine osmolarity?
So osmotic demyelination syndrome can occur both in an acute and chronic hyponatremia due to SIADH?
Bless bro 💯
thank you❤️❤️
you are the best buddy.🤭🙏
You are the best
Thanks ❤
Can we take a moment and appreciate how jacked he is , I mean , being and awesome teacher Anand a jacked man , oooh damn
Why sheehan causes effect
Why not other hypoperfusions don't cause like blood loss injuries and so
could you get renal failure in DI?
Knock knock. Who's there? Orange. Orange who?
So how do I cure this???? Please help!! It’s ruining my life
TE AMO
how to cure this disease cdi?
❤❤❤
Brother, are you ok? You have gained quite a few pounds! Cant let my teacher get unhealthy! Hope everything is ok with yo, brother!
💯🥷💯🥷💯🥷💯
Sir u can't u explain diagnostic evaluation and treatment on board y u started this new trend of teaching in computer plz stop this
Turn in to 32:53 🤦♂️
It’s the same info still… probably just easier for him
I took feel the same...
If it doesn’t work for you, don’t watch it.
This is so incredible thanks so much ❤❤
❤❤❤❤