So grateful for these kind of videos.I m from India...just got my Final year MBBS result yesterday.Passed with flying colors. Cherry on cake was I got a distinction(performed more than 75% ) in Medicine and I must say I did pick up a lot from ur video.Have been following u for a year now and never seize to surprise me with simplifying concepts and making mnemonics. Thank you so much Dirty Medicine!
They definitely used to taste the urine to see if it was sweet (G. méli: honey) or bland (L. insipidus: tasteless). Back in 1674, an English doctor by the name of Thomas Willis described the urine of a diabetic patient as "wonderfully sweet as if it were imbued with honey or sugar." It took over 100 years before the first clinical test was developed, in which a urine sample was subjected to acid hydrolysis to detect the presence of sugar. Up until that point, it was someone's job to taste a little bit of a patient's urine to determine if they had diabetes insipidus or diabetes mellitus.
fyi some boards questions also mention desmopressin test which is just an analogue of ADH. This is also used for difference between nephrogenic and central DI. If you have nephrogenic then no change with desmopressin and there will be a change in urine osmolality if central
"Diabetes" actually comes from the greek word for passing through. "Diabetes Mellitus" means passing through of something sweet and "Diabetes Insipidus" means passing through of something tasteless!
14:15 Thiazide diuretics BLOCK ( Na/Cl symporter ) in the EARLY portion of distal convoluted tubules (DCT) ===> increased electrolytes' concentration at the MACULA DENSA osmoreceptors of the DCT ===> suppression of the (Renin - angiotensin - aldosterone system) RAAS ===> reduced glomerular filtration rate (GFR) ===> reduced diuresis . The same mechanism applies to AMILORIDE which blocks sodium channels in the LATE portion of distal convoluted tubules (DCT) ===> impaired sodium reabsorption . The whole trick is about fooling the RAAS into suppressing diuresis ! ---------------------------------------------------------------------------------------------------------------------------------------------------------------- Your explanation is based on a thiazide induced hypovolemia ===> activation of RAAS ===> excessive reabsorption of water & electrolytes in the proximal convoluted tubules (PCT) ! The paradox here is that the free water loss in case of NEPHROGENIC diabetes insipidus is a way more potent to induce hypovolemia than thiazide or any other diuretic ! BTW thiazides are NOT those high ceiling diuretics to induce the desired HYPOVOLEMIA according to your explanation !
Osmoreceptor at macular densa, in this case, will secret paracrine hormone i.e. adenosine at afferent arterial to reduce blood flow . And, since it is diabetic insipidus , ANP & BNP inhibits RASS to reduce overload. The whole idea here is about how the body reduce overload by inside build-in mechanism (ANP,BNP) with (ADENOSINE,DOPAMINE).
If more water reabsorbed at PCT , then Na will be concentrated at DCT , that , will lead to auto-regulation mechanism at which the macula densa will secret paracrine adenosine at afferent arterial to be constricted to avoid hypovolemia, since RAAS is still inhibited ! The symporter at DCT will resorb Ca to stabilize hyperkalemia states i.e. seizure, muscle cramping...ect
So grateful for these kind of videos.I m from India...just got my Final year MBBS result yesterday.Passed with flying colors. Cherry on cake was I got a distinction(performed more than 75% ) in Medicine and I must say I did pick up a lot from ur video.Have been following u for a year now and never seize to surprise me with simplifying concepts and making mnemonics. Thank you so much Dirty Medicine!
Welcome to the profession.
Congratulations to you!
Congratulations
Congrats 🥂
Re-watching some of these for Step 2 --> this is just what I needed thank you!
You're the best thing that happened to USMLE step 1, cant wait to go in and Ace 260
Love these high yield series! You are a King Sir!
You are THE daddy of medicine
They definitely used to taste the urine to see if it was sweet (G. méli: honey) or bland (L. insipidus: tasteless). Back in 1674, an English doctor by the name of Thomas Willis described the urine of a diabetic patient as "wonderfully sweet as if it were imbued with honey or sugar." It took over 100 years before the first clinical test was developed, in which a urine sample was subjected to acid hydrolysis to detect the presence of sugar. Up until that point, it was someone's job to taste a little bit of a patient's urine to determine if they had diabetes insipidus or diabetes mellitus.
probably a poor M3s job
Lol 😂
@@frannytheriot that exactly what i thought🤣🤣
5th video i watched on this topic. this is the most succinct. Thank you!
Thanks!
fyi some boards questions also mention desmopressin test which is just an analogue of ADH. This is also used for difference between nephrogenic and central DI. If you have nephrogenic then no change with desmopressin and there will be a change in urine osmolality if central
DDAVP is aka desmopressin
these videos are gold not only for step-1 but also for ck and step-3.
This is really good. It answered all my questions. I had to watch this to understand my slides. Thanks for this.
Love these videos, and I love getting those juicy free points
Thanks sir! You always ROCK!
I am really appreciating your work, thank you
always I recommend people to subscribe and see your videos. thanks you soooooo much dirty.
if both urine and serum osmolarity are low that is psychogenic polydipsia
I think you should add trauma in the etiology of central diabetes inspidus
Thank you sooooo much ❤️❤️❤️🙏🙏🙏
"Diabetes" actually comes from the greek word for passing through. "Diabetes Mellitus" means passing through of something sweet and "Diabetes Insipidus" means passing through of something tasteless!
Thank you very much…made it super easy 👍
For central DI another cause could be trauma correct? Ive seen this come up a few times
yes
Due to hemorhhaging from the brain then the RAAS system being upregulated I think
@@Be1smaht interesting
Thank you for this❤
appriciate yours work
Thank you🙏
God bless you 🙏🏻
what a freaking legend
Really awesome and crystal clear concept
Super top...
In DI treatment, why does the body reacts to hypovolamia after diuretics and does not react to hypovolaemia created by DI itself?
Never seen such lecture
Tanx man, 🔥
Thank you so much sir
Tq so much
Thanks
This was amazing
🎉🎉
Thank you!!
Thank u
It's funny when you say stuff is out of the scope of STEP1 and then I get a question on it. Great vid. FUCK UWorld!
absolute legend
The link for joining dirty med community isn't opening.
How many years can live with diabetes?
Nice
🎉🎉🎉🎉
Also, bro - what happened to your twitter? You gone?
It was too redundant & time consuming for me to answer messages/emails on 4 platforms so I had to axe the one I used the least, which was Twitter
@@DirtyMedicine fair enough - I'll still share the good book of Dirty Medicine on there in your stead, tho!
Hey I'm a person who pees too much and a massive nerd. Appreciate your video
pls make video on DIURETIC DRUGS PLEASEE
What about Hypertonic Sodium solution?
???
It will supress adh will lead to diuresis nd increase in serum sodium levels
👍🏻
So grateful. .. Schwartz Batter's syndrome.
I wish you could teach me every subject
commenting for the algorithm
Your Twitter is damn good man. Keep up the good work.
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14:15 Thiazide diuretics BLOCK ( Na/Cl symporter ) in the EARLY portion of distal convoluted tubules (DCT) ===> increased electrolytes' concentration at the MACULA DENSA osmoreceptors of the DCT ===> suppression of the (Renin - angiotensin - aldosterone system) RAAS ===> reduced glomerular filtration rate (GFR) ===> reduced diuresis .
The same mechanism applies to AMILORIDE which blocks sodium channels in the LATE portion of distal convoluted tubules (DCT) ===> impaired sodium reabsorption .
The whole trick is about fooling the RAAS into suppressing diuresis !
----------------------------------------------------------------------------------------------------------------------------------------------------------------
Your explanation is based on a thiazide induced hypovolemia ===> activation of RAAS ===> excessive reabsorption of water & electrolytes in the proximal convoluted tubules (PCT) !
The paradox here is that the free water loss in case of NEPHROGENIC diabetes insipidus is a way more potent to induce hypovolemia than thiazide or any other diuretic !
BTW thiazides are NOT those high ceiling diuretics to induce the desired HYPOVOLEMIA according to your explanation !
You totally do need to know this. THANK YOU SO MUCH.
Thanks for sharing
Osmoreceptor at macular densa, in this case, will secret paracrine hormone i.e. adenosine at afferent arterial to reduce blood flow . And, since it is diabetic insipidus , ANP & BNP inhibits RASS to reduce overload. The whole idea here is about how the body reduce overload by inside build-in mechanism (ANP,BNP) with (ADENOSINE,DOPAMINE).
If more water reabsorbed at PCT , then Na will be concentrated at DCT , that , will lead to auto-regulation mechanism at which the macula densa will secret paracrine adenosine at afferent arterial to be constricted to avoid hypovolemia, since RAAS is still inhibited ! The symporter at DCT will resorb Ca to stabilize hyperkalemia states i.e. seizure, muscle cramping...ect
Thank you 🙏
Thank you!!
Thank you 🙏
Thank you ❤🙏