Thanks for the great suggestions! Jaundice will be in the next batch of "Approach to Symptom" videos, hopefully to be posted in February. I'll add the others to the list for future batches.
I have a video on the Approach to Headache that I just posted a few weeks ago. Other neuro topics are down the line, but not anticipated any time soon. It's not that they aren't important, but I try to time my videos to roughly correspond with when topics are covered in my school's curriculum. I missed the neuro block for this year already, so thus will be doing some more heme and then swinging back to cardiology.
thank you for such a nice vedio... but I have two comments : first,, in the diagram of the pathogenesis of HRS I want to say that renin-angiotensis-aldosteron works as a compensatory and work for increasing GFR because angiotensen constricts the efferent arteriol of the renal capillaries. so , althought the renal blood flow is decrease because of renal vessels constriction, the GFR is maintained because of strong contraction of efferent. artery .. and you should draw a line from ( low effective volume) directly to ( low gfr ) without passing through RAS second is hemo dyaliasis..I think you meant renal transplant,not dyaliasis ... because of course we will need hemo dyaliasis when the patient kidneys aren't going well finally, forgive me for my bad english grammmmers
Note: there is also increased activation of the sympathetic nervous system which will lead to among other things renal vasoconstriction. Also, angiotensin II does not only constrict the efferent arterioles, it also constricts the afferent arterioles just that the constriction of the efferent arterioles is more.
6:26 I didn’t understand the part that said that urine excretion of sodium is low in excessive diuresis. Aren’t the diuretics used in chronic liver disease like furosemide/spironolactone combination responsible for high urine sodium?!
@@jakedouglas6193 It's because HRS is one of the many causes of pre-renal AKI. And in pre-renal AKI the RAAS is activated and also there is increased ADH release consequently. These all lead to reabsorption of sodium in the various parts of the renal tubule together with H2O in order to preserve intravascular volume. This is the cause of the decreased urine excretion of sodium seen in HRS.
why does albumin challenge not improve renal function in HRS? albumin will increase intravascular oncotic pressure thus increase EABV, thereby reducing AKI. So how come albumin doesn't improve renal function in HRS?
@@benjaminazumah9833 I think the reason it doesn't respond to volume increases is because adding fluids would increase hepatic and splanchnic pressure and when that happens, more vasodilators are released to compensate. All the added volume goes to the splanchnic vessels and ends up causing more ascites, so the kidneys get nothing.
Sir why does Vasodilation occur in response to Portal hypertension? Is it some kind of compensatory response? Does it happen all the time? The video was awesome sir.
I was curious about this too. A quick online search indicates that it is likely a compensatory response. Endogenous vasodilators (i.e. nitric oxide) are released in an attempt to reduce vascular resistance and promote more blood flow into the portal vein.
I think It cannot and doesn't have to be like a very sharp thing but it will help me remember the concept very well. Really thankful to you brother, I will try to share some things with you if you send me your whatsapp number.
You’re a real internist. Love your work.
Thank you so much for the amazing video! You are one my top go-to sources when the books tire me out. Keep going Doc!
You are a LEGEND dr Strong. Thanks for your help. You save lives with your videos
I'm very grateful to be able to learn from your knowledge and experience. Many thanks.
I loved all of the pictures that you used to bring your points home!!!
Excellent lecture about HRS. We are grateful for your talk. It covered all the aspects
I would be interested to hear a little more about why/how the albumin challenge differentiates volume depletion from HRS.
Once Again, Great Video! Very Satisfying.
Great video as always!
Liver and kidney topics are always interesting.
Perfectly explained and very informative!
Beautifully explained
Thank you Dr Strong.
Thank you doc!
I forgot about this- thanks!
Your way of teaching is. amazing as I think is good I used from it ❤
thanks Dr Strong
Thanks!
Good job .. thank you
Thanks for the video! I have a few suggestions for the 'approach' series: jaundice, lymphadenopathy, hepatomegaly and/or splenomegaly
Thanks for the great suggestions! Jaundice will be in the next batch of "Approach to Symptom" videos, hopefully to be posted in February. I'll add the others to the list for future batches.
Thank you for the amazing video.
Will you be covering topics from neurology too?
I have a video on the Approach to Headache that I just posted a few weeks ago. Other neuro topics are down the line, but not anticipated any time soon. It's not that they aren't important, but I try to time my videos to roughly correspond with when topics are covered in my school's curriculum. I missed the neuro block for this year already, so thus will be doing some more heme and then swinging back to cardiology.
Thanks a lot sir
thanks
thank you for such a nice vedio... but I have two comments : first,, in the diagram of the pathogenesis of HRS I want to say that renin-angiotensis-aldosteron works as a compensatory and work for increasing GFR because angiotensen constricts the efferent arteriol of the renal capillaries. so , althought the renal blood flow is decrease because of renal vessels constriction, the GFR is maintained because of strong contraction of efferent. artery .. and you should draw a line from ( low effective volume) directly to ( low gfr ) without passing through RAS
second is hemo dyaliasis..I think you meant renal transplant,not dyaliasis ... because of course we will need hemo dyaliasis when the patient kidneys aren't going well
finally, forgive me for my bad english grammmmers
Note: there is also increased activation of the sympathetic nervous system which will lead to among other things renal vasoconstriction. Also, angiotensin II does not only constrict the efferent arterioles, it also constricts the afferent arterioles just that the constriction of the efferent arterioles is more.
great one...is cardio renal syndrome also planned?
I'm hoping to do a heart failure series in the spring, and if so, will be sure to incorporate this topic. Thanks for the suggestion!
@@StrongMed thx :)
6:26 I didn’t understand the part that said that urine excretion of sodium is low in excessive diuresis. Aren’t the diuretics used in chronic liver disease like furosemide/spironolactone combination responsible for high urine sodium?!
Unless you mean that on diuretics the patient has developed pre renal failure which is responsible for the low sodium.
He says low urine sodium is indicative of HRS, is this due to activation of the RAS system and resistance to diuresis that can be seen in ascites?
@@jakedouglas6193 It's because HRS is one of the many causes of pre-renal AKI. And in pre-renal AKI the RAAS is activated and also there is increased ADH release consequently. These all lead to reabsorption of sodium in the various parts of the renal tubule together with H2O in order to preserve intravascular volume. This is the cause of the decreased urine excretion of sodium seen in HRS.
Sir can u elaborate pathophysiology of anemia for us?
Hoping to start some anemia videos in Feb-March, once the cirrhosis and hemostasis series are finished.
Just watching for fun!
❤
why does albumin challenge not improve renal function in HRS? albumin will increase intravascular oncotic pressure thus increase EABV, thereby reducing AKI. So how come albumin doesn't improve renal function in HRS?
Because in HRS, patients are "volume non-responsive" in the first place.
@@benjaminazumah9833 I think the reason it doesn't respond to volume increases is because adding fluids would increase hepatic and splanchnic pressure and when that happens, more vasodilators are released to compensate. All the added volume goes to the splanchnic vessels and ends up causing more ascites, so the kidneys get nothing.
Sir why does Vasodilation occur in response to Portal hypertension? Is it some kind of compensatory response? Does it happen all the time?
The video was awesome sir.
I was curious about this too. A quick online search indicates that it is likely a compensatory response. Endogenous vasodilators (i.e. nitric oxide) are released in an attempt to reduce vascular resistance and promote more blood flow into the portal vein.
Oh wowow Thanks a lot brother. Can I have your whatsapp number if you don't mind.
I think It cannot and doesn't have to be like a very sharp thing but it will help me remember the concept very well. Really thankful to you brother, I will try to share some things with you if you send me your whatsapp number.
coz o liver is not able to metabolize NO thatswhy splanchnic vasodiltion occurs
Will the Abdominal X-Ray series be forthcoming?
I know...I've been meaning to cover that topic for 2 years now. Hoping to get to it in the next couple of months, but no guarantees.
A complication is sometimes... death.