Hello, I am a Paramedic in NJ. I randomly chose a video to post under, but I have spent countless hours reviewing your videos, often taking notes, to help the night pass by during "downtime". Thank you for the commitment you've made to making them.
Thank you so much for helping me understand the finer aspects of renal physiology! I HATED it as an undergrad as i didn't understand it. Now as a Masters student, i had no choice but to learn... thanks so much!
Your videos are very helpful. I am a paramedic and RN and they have increased body understanding of so many body systems. I appreciate your investment of time and hope to see more videos!! Thank you!!
i do appreciate of your work, understand it more,but i am not pretty clear about mesangial physiology! i wish i can see it more from your video! oh,if it possible for you to upload the pulmonary disorder and its pathophysiology? i think i am capable to understand by your video than other's. thanks before hands!
From all sources I've gathered concerning this, only similar thing ive found is stage one. The rest of the stages are different from every source and now i don't know what is true and what is not😳
would it be possible for you to create a video dealing with URINALYSIS? and what type of findings would you expect to find in urine dipstick and under microscope for a patient with different types of renal disease, such as glumerolonephritis, TN, diabetic nephropathy and others? IT WOULD BE MOST APPRECIATED
Thanks for this very good presentation of the mechanism of diabetic nephropathy but it will be good if you include treatment of different stages of diabetic nephropathy .
my second question is that we classify renal failure into 5 main classes according to the GFR of the patient in CKD 5 the GFR is less the 15ml/min so will all these patient's develop uremic syndrome?
Hello, first of all great videos thank you! My question is about the 5 stages.....at stage 2 you said that people will start developing proteinuria does that also correlate to the GFR being mildly decreased? Along with stage 3 and the hematuria will the GFR be moderately decreased?
what is the role of podocytes in the pathophysiology of diabetic nephropathy.?? and please can u suggest the recent globally accepted classification of diabetic nephropathy
That explains it in type 2 diabetes. Type 1 is as I'm sure you know characterized by complete lack of insulin. And yet they develop diabetic nephropathy just as well. In type 2s it is due to a heterogenous group of diseases, dislipidemias, HTN...in addition to to diabetes. In type 1 there is only one initiating factor -that it shares with type 2. Is it the effect of hyperglycemia that causes the nephropathy in this case?
HI i found your video quite helpful. but was wondering if you could explain kamilstain wilson lesion/nodule my interpretation of it is because of increased mesangial proliferation in response to mesangial and glommerular dammage the mesangial cells proliferate and eventually form small nodules known as kamelstein wilson nodules? wondering if i'm correct cheers
Hi. Is the biggest cause of Diabities high blood sugar and high glucose. Does the High Bp damages the blood vessels of the kidneys leaving them ineffective over long period of high bp?
In diabetes type 2 there is a decreased sensitivity and so increased resistance to insulin causing the beta cells of the pancreas to secrete more insulin. That is why often their treatment initially involves drugs that increase sensitivity or decrease resistance, but due to continuous stimulation of the beta cells at some point they get damaged and exhausted, and treatment then often includes insulin therapy. atleast that what I understand from it..
Also why does the efferent arteriole constrict? you mentioned free radicals, but what is the reasoning for the efferent arteriole wanting to constrict? or why do the free radicals cause this?
Just to add to the wonderful explanation: Increase in GFR initially is caused due to hyalinization of efferent arteriole,which causes vasoconstriction---predisoposes to hyperfilteration injury Meanwhile non enymatic glycosylation of the basement membrane of the glomerules causes injury and leads to proteinuria esp. called as microalbuminuria. ACE inhibitiors prevent the cond'n as efferent arterilole are under Angiotensin 2 control,which causes vasoconstriction, thus giving an ACE would cause dilation of the hyalinzed efferent arteriole nd improve the GFR as well as hyperfilteraion injury.
ace inhibitor works on those with this condition provided that the dose is higher than normal and creatinine is between 1.3 to 2.0. it can completely reverse it at those levels with no need for dialysis later on.
Where have you been all this time? Your videos are so simple to understand and I understand the information much better than when I read my books :-)
Hello. Ur fan from India. Very thankful for ur efforts. GOD bless u :)
This was SO HELPFUL!!!
Hello, I am a Paramedic in NJ. I randomly chose a video to post under, but I have spent countless hours reviewing your videos, often taking notes, to help the night pass by during "downtime". Thank you for the commitment you've made to making them.
Thanks for your feedback and thank you for watching.
Thank you so much for helping me understand the finer aspects of renal physiology! I HATED it as an undergrad as i didn't understand it. Now as a Masters student, i had no choice but to learn... thanks so much!
You're welcome!
Your videos are very helpful. I am a paramedic and RN and they have increased body understanding of so many body systems. I appreciate your investment of time and hope to see more videos!! Thank you!!
Thanks for your feedback and thank you for watching.
thank you very much Dr. Andrew, the video is explained properly
You're welcome!
Complex topic simplified to a considerable extent.
Thanks for the feedback!
great video :-)
thank you for the great explanation! Your videos are very helpful.
You're welcome!
i do appreciate of your work, understand it more,but i am not pretty clear about mesangial physiology! i wish i can see it more from your video! oh,if it possible for you to upload the pulmonary disorder and its pathophysiology? i think i am capable to understand by your video than other's. thanks before hands!
From all sources I've gathered concerning this, only similar thing ive found is stage one. The rest of the stages are different from every source and now i don't know what is true and what is not😳
thank a lot sharing yours knowledge
You're welcome!
solid,,absolutely clear
Thank you so much!
Could you go more in depth into how hyperglycemia damages the nephron?
would it be possible for you to create a video dealing with URINALYSIS? and what type of findings would you expect to find in urine dipstick and under microscope for a patient with different types of renal disease, such as glumerolonephritis, TN, diabetic nephropathy and others? IT WOULD BE MOST APPRECIATED
Thanks for this very good presentation of the mechanism of diabetic nephropathy but it will be good if you include treatment of different stages of diabetic nephropathy .
Appreciate the feedback!
Thank you so much,this was pretty helpful
You're welcome!
Man you are awesome i love you ! :)
Thanks for your feedback and thank you for watching.
thanks for this great and helpful information but i got a question please , does hypertensive nephropathy affect mesangium ? and if not ,why?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
That was so clear thank you so much
You're welcome!
my second question is that we classify renal failure into 5 main classes according to the GFR of the patient in CKD 5 the GFR is less the 15ml/min so will all these patient's develop uremic syndrome?
Hello, first of all great videos thank you! My question is about the 5 stages.....at stage 2 you said that people will start developing proteinuria does that also correlate to the GFR being mildly decreased? Along with stage 3 and the hematuria will the GFR be moderately decreased?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
Thank you, this was so useful :)
You're welcome!
subscribing ! :)
Thank you for your videos. do you have a video about chronic kidney disease?
Thanks Richel for the support. More videos being released weekly!
what is the role of podocytes in the pathophysiology of diabetic nephropathy.?? and please can u suggest the recent globally accepted classification of diabetic nephropathy
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
That explains it in type 2 diabetes. Type 1 is as I'm sure you know characterized by complete lack of insulin. And yet they develop diabetic nephropathy just as well. In type 2s it is due to a heterogenous group of diseases, dislipidemias, HTN...in addition to to diabetes. In type 1 there is only one initiating factor -that it shares with type 2. Is it the effect of hyperglycemia that causes the nephropathy in this case?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
HI i found your video quite helpful. but was wondering if you could explain kamilstain wilson lesion/nodule my interpretation of it is because of increased mesangial proliferation in response to mesangial and glommerular dammage the mesangial cells proliferate and eventually form small nodules known as kamelstein wilson nodules? wondering if i'm correct
cheers
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
@@HealthEdSolutions are you for real fool. I posted that question almost 10 years ago. I am a specialist doctor now.
Are all the functions of human kidneys basically the same in animals such as fish, dogs, cattle birds and other animals?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
Hi. Is the biggest cause of Diabities high blood sugar and high glucose. Does the High Bp damages the blood vessels of the kidneys leaving them ineffective over long period of high bp?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
In diabetes type 2 there is a decreased sensitivity and so increased resistance to insulin causing the beta cells of the pancreas to secrete more insulin. That is why often their treatment initially involves drugs that increase sensitivity or decrease resistance, but due to continuous stimulation of the beta cells at some point they get damaged and exhausted, and treatment then often includes insulin therapy.
atleast that what I understand from it..
Also why does the efferent arteriole constrict? you mentioned free radicals, but what is the reasoning for the efferent arteriole wanting to constrict? or why do the free radicals cause this?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
@@HealthEdSolutions I asked EIGHT... YEARS... AGO... lol...
Could you please tell me how non enzymatic glycosylation and hyaline arteriolosclerosis relate to diabetic nephropathy?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
Thank you :)
You're welcome!
you rock !
Appreciate the support!
why there is increased level of angiotensin 2 in DM?
Thanks so much for your inquiry. We have passed this question on to our medical review team. Thanks again for watching!
You ARE A-Mazing
Thanks for your feedback and thank you for watching.
Just to add to the wonderful explanation:
Increase in GFR initially is caused due to hyalinization of efferent arteriole,which causes vasoconstriction---predisoposes to hyperfilteration injury
Meanwhile non enymatic glycosylation of the basement membrane of the glomerules causes injury and leads to proteinuria esp. called as microalbuminuria.
ACE inhibitiors prevent the cond'n as efferent arterilole are under Angiotensin 2 control,which causes vasoconstriction, thus giving an ACE would cause dilation of the hyalinzed efferent arteriole nd improve the GFR as well as hyperfilteraion injury.
ace inhibitor works on those with this condition provided that the dose is higher than normal and creatinine is between 1.3 to 2.0. it can completely reverse it at those levels with no need for dialysis later on.
Thanks for the wonderful input
Appreciate the comment on this
vasoconstriction of efferent arterioles decrease glumerular pressure and filtration
Thanks for your input!
sound?