Watched your videos as a student, watched them as an intern, now watching them as a house officer in nephrology :'). You are truly something special Dr. Bolin.
Watching them as someone born with ARPKD (now with PMOD) and a current creatnine of 280, planning to surprise my nephrologist with some higher-level understanding of my condition! :)
19:11 Cause some may find it confusing: Damaged adrenal glands --> no cortisol etc. --> lack of cortisol etc. means lack of negative feedback to hypothalamus --> a not inhibited hypothalamus releases CRH --> CRH stimulates pituitary to release ACTH + MSH as a byproduct --> MSH stimulates melanocytes --> hyperpigmentation. 21:31 An update: AFAIK hepatorenal syndrome is caused (very simplified) by a cirrhotic liver releasing substances as NO that will lead to vasodilation in the splanchnic system --> blood is missing then in the periphery --> decreased renal perfusion --> release of renin, etc.
Medical therapy - Bilateral renal hypoperfusion induces activation of the renin-angiotensin-aldosterone system and impairs sodium excretion resulting in expansion of the extracellular fluid volume. Both of these factors contribute to the ensuing rise in blood pressure. As a result, combination therapy with a diuretic plus an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) can control the hypertension in most patients with bilateral renal artery stenosis and is likely to be more effective than other antihypertensive therapy. In a Canadian cohort study, for example, patients with renal artery stenosis who were prescribed ACE inhibitors were significantly less likely to die or have a myocardial infarction or stroke (10 versus 13 events per 100 patient-years) as compared with similar patients prescribed other therapy [18]. ACE inhibitor therapy was also associated with a lower risk of end-stage renal disease but a higher risk of acute kidney injury (1.2 versus 0.6 events per 100 patient-years). This is from uptodate. 2016
@ 19:11 - CRH acts on the corticotrophs of the Anterior pituitary to synthesize POMC (Proopiomelanocortin)...ACTH and MSH are by products of POMC..ACTH goes on to simulate the adrenals and msh goes on to stimulate melanocytes.
Thanks for everything...Just a comment: In hypoaldosteronism, I would assume that the criteria of prerenal failure are not met as FEna will be high due to the absence of Aldosterone. Am I getting this right?
Watched your videos as a student, watched them as an intern, now watching them as a house officer in nephrology :'). You are truly something special Dr. Bolin.
Watching them as someone born with ARPKD (now with PMOD) and a current creatnine of 280, planning to surprise my nephrologist with some higher-level understanding of my condition! :)
19:11 Cause some may find it confusing:
Damaged adrenal glands --> no cortisol etc. --> lack of cortisol etc. means lack of negative feedback to hypothalamus --> a not inhibited hypothalamus releases CRH --> CRH stimulates pituitary to release ACTH + MSH as a byproduct --> MSH stimulates melanocytes --> hyperpigmentation.
21:31 An update: AFAIK hepatorenal syndrome is caused (very simplified) by a cirrhotic liver releasing substances as NO that will lead to vasodilation in the splanchnic system --> blood is missing then in the periphery --> decreased renal perfusion --> release of renin, etc.
I absorbe your lectures just like sponge absorbes water, thank you sir!
Medical therapy - Bilateral renal hypoperfusion induces activation of the renin-angiotensin-aldosterone system and impairs sodium excretion resulting in expansion of the extracellular fluid volume. Both of these factors contribute to the ensuing rise in blood pressure. As a result, combination therapy with a diuretic plus an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) can control the hypertension in most patients with bilateral renal artery stenosis and is likely to be more effective than other antihypertensive therapy. In a Canadian cohort study, for example, patients with renal artery stenosis who were prescribed ACE inhibitors were significantly less likely to die or have a myocardial infarction or stroke (10 versus 13 events per 100 patient-years) as compared with similar patients prescribed other therapy [18]. ACE inhibitor therapy was also associated with a lower risk of end-stage renal disease but a higher risk of acute kidney injury (1.2 versus 0.6 events per 100 patient-years).
This is from uptodate. 2016
@ 19:11 - CRH acts on the corticotrophs of the Anterior pituitary to synthesize POMC (Proopiomelanocortin)...ACTH and MSH are by products of POMC..ACTH goes on to simulate the adrenals and msh goes on to stimulate melanocytes.
10:01 that would be Angiotensin II, not Aldosterone!
Dude ,tks for the help in nephrology !!!
To be honest, I repeated this lecture 3 times to understand :-)
Thank you!
Kindly upload your slides in a PDF form, please :)!
Thank you
Legend Dr Bolin MD
Thanks for everything...Just a comment: In hypoaldosteronism, I would assume that the criteria of prerenal failure are not met as FEna will be high due to the absence of Aldosterone. Am I getting this right?
Ghada Aborkhees same Q
Thanks
But does aldostrone or angiotensin 2 are the cause of constiction in effernt areteriole??
I understand why we don’t give ACE inhibitors to patients with bilateral renal artery stenosis; what about unilateral RAS?
the contraindication is bilateral not unilateral!!!
@Mohiuddin -- my question is, why is it ok for unilateral?
@@T83854 I guess because you have a backup. Ah, you mean why it won't lead to unilateral AKI then?
@5:20 I assume you are saying Control Hypertension, Instead of controlling LDL