My son PGH is 5 years old and has antenatal bartter syndrome. He was born premature, stayed at the NICU for 3 months..Today, we r at a mission of sharing my sons life to make people more aware of this illness...
VERY NICE writing the facts explaining the pathophysiology behind and relating facts to clinical scenarios and clinical histories. no way you can forget . i think his lectures are better than books. no need to make page memories and mneumonics or diagram. his lectures have nice histories. thank you sir
I had a doubt:- you mentioned that it is associated with hypokalemia which seems befitting according to the explanation given but Ganong mentions that there is hyperkalemia.. Could you pls clarify that. Thankyou.
Hi thank you for the extremely useful video for Batter syndrome. I would like to highlight the following, according to my understanding: 1. ROMK channel malfunction will cause hyperkalaemia, since normal function is to excrete potassium, hence initially can see hyperkalaemia but cotransporter also loses it from the Na2clk cotransproter hence there is no net gain or loss. 2. The main mechanism is from secondary aldosteronsim and metabolic alkalosis causing potassium wasting leading to hypokalaemia. Please correct me if I am wrong.
Hello sir. Good greetings. I think ROMK transports K+ from the lumen of LoH to the cells so it can be put back into blood stream. So when ROMK is defective, there will be loss of K+ in the urine causing HYPOkalaemia and not HYPERkalaemia.
Hello Doctor, If you are a premium user, you can directly ask doubts from our faculty using the 'Ask Doubt' section available in the sidebar of the PrepLadder application.
Na±K+2Cl cotransporter causes reabsorption of the mentioned ions and water follows these ions; in bartter's syndrome, there is loss of function of na,k,cl cotransporter and thus water too cannot be reabsorbed from urine-≥ urine osmolality reduces
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My son PGH is 5 years old and has antenatal bartter syndrome. He was born premature, stayed at the NICU for 3 months..Today, we r at a mission of sharing my sons life to make people more aware of this illness...
Apka baby thik he Abhi??
I met a girl 23 year old known case of barter.
She was treated with indomethacin.
Now living a normal life.
She has Normal development.
Superb, Brilliant, Excellent, Phenomenal 😊😊
I have got excellent understanding through your lectures.. Very well appreciated.. Thanks a alot sir
VERY NICE writing the facts explaining the pathophysiology behind and relating facts to clinical scenarios and clinical histories. no way you can forget . i think his lectures are better than books. no need to make page memories and mneumonics or diagram. his lectures have nice histories. thank you sir
Perfectly said👍
You made it a piece of cake for me. Tysm.
Thankyu sir for such an amazing lecture
Thank you! That was extremely well explained!
You
Superb sir please upload more topics
Very helpful sir
thankyu sir
Sir please can u help me ...
About which topics should be much focused for NEET xm
thanks a lot.
Superb sir
Superb
tq
Sir, thick ascending limb is water impermeable. Chloride channels are situated on basolateral side. As I know.
Pls correct me sir. Whether I am wrong?
You're correct Thick ascending limb is impermeable to water
2 sodium pottasium chloride channel is present in apical side
sir very nice
WHY WOULD URINARY OSMOLALITY BE LOW, AINCE THERE IS ELECTROLYTE LOSS, SHOULD IT NOT BE HIGH ???
I had a doubt:- you mentioned that it is associated with hypokalemia which seems befitting according to the explanation given but Ganong mentions that there is hyperkalemia.. Could you pls clarify that. Thankyou.
As thick loop has na k 2 cl transporter channel....the defect in this channel wd lower down All these 3 electrolytes....
Hi thank you for the extremely useful video for Batter syndrome. I would like to highlight the following, according to my understanding:
1. ROMK channel malfunction will cause hyperkalaemia, since normal function is to excrete potassium, hence initially can see hyperkalaemia but cotransporter also loses it from the Na2clk cotransproter hence there is no net gain or loss.
2. The main mechanism is from secondary aldosteronsim and metabolic alkalosis causing potassium wasting leading to hypokalaemia.
Please correct me if I am wrong.
Hello sir. Good greetings.
I think ROMK transports K+ from the lumen of LoH to the cells so it can be put back into blood stream. So when ROMK is defective, there will be loss of K+ in the urine causing HYPOkalaemia and not HYPERkalaemia.
ROMK will direct pottaisum into blood
Usually it will prevent pottasium loss
So if it is defective it will cause potassium loss in urine
HYPOKALEMIA
i have bartter syndrome and it really sucks!!
Rx- K+ supplements, Amiloride, Indomethacin
🤩
Why is urine osmolality low?
Hello Doctor,
If you are a premium user, you can directly ask doubts from our faculty using the 'Ask Doubt' section available in the sidebar of the PrepLadder application.
Na±K+2Cl cotransporter causes reabsorption of the mentioned ions and water follows these ions; in bartter's syndrome, there is loss of function of na,k,cl cotransporter and thus water too cannot be reabsorbed from urine-≥ urine osmolality reduces
Yes very nice video my son have this disease i am in Spain
My son also have burter,my son is 3 years old....
My son to have same disease what kind of treatment should be taken to cure if anyone knows about plz just tell me