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.
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.
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.
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.
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.
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