MrBhotu, I'm glad you have enjoyed the videos. I'm working on the remaining lectures of the ABG series as fast as I can, but unfortunately I don't have time built into my work schedule for this, so I can only do a little here and there. I hope to finish ABG lectures 11-20 by mid summer.
awesome videos ...please upload the later parts....i am starving to see them dr eric...excellent presentation .......this is real teaching ....many many thanks sir ...looking for parts on lecture 11 and onwards
great lectures sir, they are presented just the way anybody understands! thank you very much.... looking for the lectures 11 to 15... hope you have not forgotten them!(as 16 and 17th lectures are already uploaded).
Hi, I agree with Asha Krishnaq who ask about renal failure because after all these lectures about ABG, we are almost ready to digest a not easy topic like Kidney disease.. I really enjoy these lectures, i feel like I can master evrything after that now
This is an old comment, but I'll answer anyway: Cortisol is structurally related to aldosterone and can also bind to mineralocorticoid receptors (aldosterone receptors) so that it causes, among other things, sodium and water retention as well.
@@christineschilde5055 I fully agree with you that glucocorticoids like cortisol have mineralocorticoid - like actions as that of aldosterone ; where both of them share the chemical structural similarity of STEROIDS . My question focuses on feedback loops in case of salt & water retention ; primarily (renin - angiotensin - aldosterone axis) . That axis is supposed to be SUPPRESSED in case of hypervolemia ! Even if we go with the final algorithm of metabolic alkalosis , we will find Cushing syndrome associated with HYPERTENSION , a well known suppressor of that axis ! So , how comes we get NORMAL levels of renin & aldosterone in case of Cushing syndrome ? Thanks for the comment anyway !
@@WhyNot-si4pj Oh okay, I see where you're coming from. I think, whereas HYPOvolemia, HYPOnatremia and drops in blood pressure (developing HYPOtension) are indeed stimuli for the release of renin, the same does not count for the other way around - the inhibiting role - meaning that HYPERtension and HYPERnatremia don't act automatically as blockers of the renin release. It is really bound to Angiotensin II and Aldosteron (mineralocorticoids) to cause LESS renin output in that axis. Glucocorticoids/cortisol is quite independent from that. This is my kind of understanding of it.
@@christineschilde5055 Thank you again for the reply ! Hypertension by itself is associated by an excessive adrenergic activity leading to stimulation of the B1 receptors in the JG cells ==> activation of (RAAS) ! That's why it overrides the normal inhibition associated with increased filteration pressure & increased delivery of electrolytes to the osmoreceptors of macula densa supposed to ==> inhibition of (RAAS) . Even in chronic hypertension ; local autoregulatory mechanisms for blood flow sets in to counteract the increased renal blood flow associated with hypertension ! That includes local arterial vasoconstriction up to hyperplastic arteriosclerosis ! Remember the shrunk , flea bitten appearance of hypertensive kidney in gross pathology ! d1yboe6750e2cu.cloudfront.net/i/ff4a8e41785f060a45d5f669091f408dfcc2a7ed
@@christineschilde5055 I believe I reached a good explanation for the normal levels of renin & aldosterone in case of Cushing syndrome ! The high levels of cortisol results in increased sympathetic activity leading to stimulation of the B1 receptors in the JG cells ==> activation of (RAAS) ! That counteracts the reduction of renin & aldosterone levels associated with salt & water retention !
I have a question,when someone uses loop or thiazide duretics it prevents sodium and water reabsorbtion and so increases the tubular flow to macula densa cells,so macula densa cells should falsely sense an Increased GFR and decrease Renin secretion results in decreased aldosteron and Ag2.whay we seeing oposite to that?
In case of using loop diuretics or thiazide diuretics the unabsorbed sodium in the proximal portions of the nephron will be referred to the late DCT & collecting tubules ; resulting in excessive sodium reabsorption down gradiently to the hypoosmolal interstitium created by the diuretics & independently from aldosterone action ! Of course initially excessive delivery of electrolytes at the macula densa would falsely sense an increased GFR with subsequent SUPPRESSION of (RAAS) ; but later on the resulting hypovolemia in the course diuretic use would result in reduced stimulation of the stretch receptors of the JG cells leading to increased Renin secretion & activation of (RAAS) !
Thank you for your Lectures! I know, from a previous lecture, that you dislike mnemonics. However, I wonder if there is a "Best" one for non-anion gap acidosis? The one I found, which I like (so far), is ABCD A - Addisons B - Bicarb Loss C - Chloride Excess D - Drugs Bicarb loss covers RTA (which gets me thinking of all types of RTA), Diarrhea, and Fistula Chloride excess covers the infusion of saline, etc. Your thoughts?
Mike Birkhead The one I was taught was HEART CCU (as in, the cardiac critical care unit) H Hyperkalemia E Expansion (infusion of saline) A Alimentation (overeating, parental overnutrition) R Renal Tubular Acidosis (Types I, II, or IV), Renal Failure T Trots (gastrointestinal loss) C Cholestyramine C Carbonic Anhydrase Inhibitors (acetazolamide) U Ureteral diversion
Mike Birkhead I''m so sorry, I didn't see your original comment until @samblack just replied. You're correct, I'm not a fan of mnemonics, and thus, don't have a favorite. The one for normal gap acidosis that I was taught in med school was "HARD UP": hyperalimentation, acetazolamide, renal failure/RTA, diarrhea, ureteral diversion, and pancreatic fistula. But this misses a major etiology - excessive infusion of normal saline. I think any mnemonic is probably fine, as long as it somehow includes RTA, renal failure, diarrhea, and normal saline (which collectively are probably responsible for >99% of cases)
Great.but i want To know bow is it possible that volume depletion can cause contraction alcalose and acidose at the same time?we know that when we have hypoperfusion we have production of lactic acid in the tissus
That's a good question. Essentially, when volume depletion is mild, the renin-angiotensin-aldosterone system is able to compensate enough to maintain a blood pressure high enough to perfusion your organs and tissues, but at the cost of a metabolic alkalosis. But once volume depletion becomes severe enough that hypotension leads to hypoperfusion, you develop lactic acidosis that is more pronounced in its pH effect than the mild alkalosis that preceded it.
Hi Eric, Thanks for the nice well put together talk, I wonder if you can make a comment about treatment of Metabolic Alkalosis where no reversible cause is obvious or when it is very Severe? What about using Acetazolamide to mitigate the situation in severe cases. Many Thanks
Dr. Strong, thank you for answering my previous question. I have another question that maybe you would be able to answer. In response to low blood pressure, why does ATII and aldosterone increase H+ secretion and HCO3- reabsorption respectively? It seems odd to me that pH is addressed in conjunction with blood pressure. It seems to me that increasing pH would have little to no effect on increasing blood volume.
" In response to low blood pressure , why does ATII and aldosterone increase H+ secretion and HCO3- reabsorption respectively? " !! AT II promotes HCO3 - reabsorption in PCT ; while aldosterone promotes H+ secretion in the late DCT & collecting tubules with a net result of CONTRACTION ALKALOSIS ! My humble understanding of the conjunction between the drop in BP & the rise in pH is that it's a kind of compensatory mechanism ; where drop in BP ==> tissue hypoperfusion ==> cellular switch to anaerobic metabolism ==> lactic acidosis ==> elevated AG metabolic acidosis ! So contraction alkalosis helps rapidly mitigate the effects of low pH on the vital organs like CNS & heart ! Lord knows best !
For your slide @15 min, why is Cushing Syndrome included in causes of mineralocorticoid excess. Isn't Cushing Syndrome an increase of cortisol which is a glucocorticoid?
Although cortisol is classified as a glucocorticoid, it has some mineralocorticoid activity. Here's an article that discusses some of the relevant physiology: www.karger.com/Article/FullText/314315
@@StrongMed Thank you. Lots of great info in this article. I was surprised to learn that cortisol activates the RAAS (something they don't teach us in med school)
@@TheSpades21 I read in that paper dating to 2010 that cortisol enhances (RAAS) despite plasma renin activity and plasma renin concentration are generally normal or suppressed in patients with CS ! Does this make any sense ?
Thanks for your comment. Unfortunately, there are no immediate plans to discuss treatment options here - too many other requested topics... Hopefully, someday I can circle around to the acid-base topics again.
I'm carnivore and don't eat carbs at all. ZERO carbs. Recently, I was sick with a virus. Just before, what I thought was full recovery, I became very weak. I suddenly needed sugar. I ate three packets of sugar and a Snickers Bar and soon felt better. When I got home, I ate two bowls of icecream. The next day, I was still a little weak so I had a small bowl of icecream and a prtein shake. Less than an hour later, I was in the Emergency Room. There, I was given three IV bags and two big Potassium pills. I was told that my Potassium was low, which I found strange because I salt my meat with a 50/50 blend of NaCl and Potassium Citrate. I actually had an electrlyte drink that morning. My discharge papers say Accute Respiratory Alkalosis but I can't help but think that it was more due to my etreme insulin sensitivity and my sugar intake. I wasn't haveing diarrhea and only vomited once. Potassium being low makes me think that it wasn't Milk-Alkali Syndrome but all that icecream that I consumed makes me wonder. 3 weeks prior, my Potassium was 4.9.
Lectures 11-15 are still coming. I was getting a little acid-base fatigued so decided to mix it up with some oxygenation for a couple lectures.
MrBhotu, I'm glad you have enjoyed the videos. I'm working on the remaining lectures of the ABG series as fast as I can, but unfortunately I don't have time built into my work schedule for this, so I can only do a little here and there. I hope to finish ABG lectures 11-20 by mid summer.
12 years ahve passed , still this video is the best one explaining alkalosis, hats off to u
awesome videos ...please upload the later parts....i am starving to see them dr eric...excellent presentation .......this is real teaching ....many many thanks sir ...looking for parts on lecture 11 and onwards
great lectures sir, they are presented just the way anybody understands! thank you very much....
looking for the lectures 11 to 15... hope you have not forgotten them!(as 16 and 17th lectures are already uploaded).
What does hypercalcaemia have to do with metabolic alkalosis
Hi, I agree with Asha Krishnaq who ask about renal failure because after all these lectures about ABG, we are almost ready to digest a not easy topic like Kidney disease..
I really enjoy these lectures, i feel like I can master evrything after that now
2:50 Contraction alkalosis
8:09 Diuretics
-Volume contraction
10:27 Vomitting
Nasogastric suction
10:52 Mineralocorticoid excess
15:31 Hypokalemia
16:07 Milk-Alkali syndrome
16:58 Bartter & Gitelman syndrome
What does urinary chloride levels has to do with metabolic alkalosis?
What makes it chloride resistant or chloride responsive?
Thank you Dr Eric Strong. Good lecture.
The best ever explanation
this is perfect, just what i needed! thank you :)
19:56 Why is Cushing syndrome associated with normal levels of renin & aldosterone though it results in volume expansion ?
This is an old comment, but I'll answer anyway: Cortisol is structurally related to aldosterone and can also bind to mineralocorticoid receptors (aldosterone receptors) so that it causes, among other things, sodium and water retention as well.
@@christineschilde5055 I fully agree with you that glucocorticoids like cortisol have mineralocorticoid - like actions as that of aldosterone ; where both of them share the chemical structural similarity of STEROIDS . My question focuses on feedback loops in case of salt & water retention ; primarily (renin - angiotensin - aldosterone axis) . That axis is supposed to be SUPPRESSED in case of hypervolemia ! Even if we go with the final algorithm of metabolic alkalosis , we will find Cushing syndrome associated with HYPERTENSION , a well known suppressor of that axis ! So , how comes we get NORMAL levels of renin & aldosterone in case of Cushing syndrome ? Thanks for the comment anyway !
@@WhyNot-si4pj Oh okay, I see where you're coming from. I think, whereas HYPOvolemia, HYPOnatremia and drops in blood pressure (developing HYPOtension) are indeed stimuli for the release of renin, the same does not count for the other way around - the inhibiting role - meaning that HYPERtension and HYPERnatremia don't act automatically as blockers of the renin release. It is really bound to Angiotensin II and Aldosteron (mineralocorticoids) to cause LESS renin output in that axis. Glucocorticoids/cortisol is quite independent from that. This is my kind of understanding of it.
@@christineschilde5055 Thank you again for the reply ! Hypertension by itself is associated by an excessive adrenergic activity leading to stimulation of the B1 receptors in the JG cells ==> activation of (RAAS) ! That's why it overrides the normal inhibition associated with increased filteration pressure & increased delivery of electrolytes to the osmoreceptors of macula densa supposed to ==> inhibition of (RAAS) . Even in chronic hypertension ; local autoregulatory mechanisms for blood flow sets in to counteract the increased renal blood flow associated with hypertension ! That includes local arterial vasoconstriction up to hyperplastic arteriosclerosis !
Remember the shrunk , flea bitten appearance of hypertensive kidney in gross pathology !
d1yboe6750e2cu.cloudfront.net/i/ff4a8e41785f060a45d5f669091f408dfcc2a7ed
@@christineschilde5055 I believe I reached a good explanation for the normal levels of renin & aldosterone in case of Cushing syndrome ! The high levels of cortisol results in increased sympathetic activity leading to stimulation of the B1 receptors in the JG cells ==> activation of (RAAS) ! That counteracts the reduction of renin & aldosterone levels associated with salt & water retention !
many thanks 4 you really great work and in a very simple way .
I need you to also add how to treat at the end of these treasures lectures
I have a question,when someone uses loop or thiazide duretics it prevents sodium and water reabsorbtion and so increases the tubular flow to macula densa cells,so macula densa cells should falsely sense an Increased GFR and decrease Renin secretion results in decreased aldosteron and Ag2.whay we seeing oposite to that?
In case of using loop diuretics or thiazide diuretics the unabsorbed sodium in the proximal portions of the nephron will be referred to the late DCT & collecting tubules ; resulting in excessive sodium reabsorption down gradiently to the hypoosmolal interstitium created by the diuretics & independently from aldosterone action ! Of course initially excessive delivery of electrolytes at the macula densa would falsely sense an increased GFR with subsequent SUPPRESSION of (RAAS) ; but later on the resulting hypovolemia in the course diuretic use would result in reduced stimulation of the stretch receptors of the JG cells leading to increased Renin secretion & activation of (RAAS) !
Thank you for your Lectures!
I know, from a previous lecture, that you dislike mnemonics. However, I wonder if there is a "Best" one for non-anion gap acidosis?
The one I found, which I like (so far), is ABCD
A - Addisons
B - Bicarb Loss
C - Chloride Excess
D - Drugs
Bicarb loss covers RTA (which gets me thinking of all types of RTA), Diarrhea, and Fistula
Chloride excess covers the infusion of saline, etc.
Your thoughts?
Mike Birkhead The one I was taught was HEART CCU (as in, the cardiac critical care unit)
H Hyperkalemia
E Expansion (infusion of saline)
A Alimentation (overeating, parental overnutrition)
R Renal Tubular Acidosis (Types I, II, or IV), Renal Failure
T Trots (gastrointestinal loss)
C Cholestyramine
C Carbonic Anhydrase Inhibitors (acetazolamide)
U Ureteral diversion
Mike Birkhead I''m so sorry, I didn't see your original comment until @samblack just replied. You're correct, I'm not a fan of mnemonics, and thus, don't have a favorite. The one for normal gap acidosis that I was taught in med school was "HARD UP": hyperalimentation, acetazolamide, renal failure/RTA, diarrhea, ureteral diversion, and pancreatic fistula. But this misses a major etiology - excessive infusion of normal saline. I think any mnemonic is probably fine, as long as it somehow includes RTA, renal failure, diarrhea, and normal saline (which collectively are probably responsible for >99% of cases)
thank you Mr. Strong, I like this lecture most.
Great.but i want To know bow is it possible that volume depletion can cause contraction alcalose and acidose at the same time?we know that when we have hypoperfusion we have production of lactic acid in the tissus
That's a good question. Essentially, when volume depletion is mild, the renin-angiotensin-aldosterone system is able to compensate enough to maintain a blood pressure high enough to perfusion your organs and tissues, but at the cost of a metabolic alkalosis. But once volume depletion becomes severe enough that hypotension leads to hypoperfusion, you develop lactic acidosis that is more pronounced in its pH effect than the mild alkalosis that preceded it.
@@StrongMed thanks a lot for the answer
what is the relation between metabolic alkalosis and renal failure
Hi Eric, Thanks for the nice well put together talk, I wonder if you can make a comment about treatment of Metabolic Alkalosis where no reversible cause is obvious or when it is very Severe? What about using Acetazolamide to mitigate the situation in severe cases. Many Thanks
Dr. Strong, thank you for answering my previous question. I have another question that maybe you would be able to answer. In response to low blood pressure, why does ATII and aldosterone increase H+ secretion and HCO3- reabsorption respectively? It seems odd to me that pH is addressed in conjunction with blood pressure. It seems to me that increasing pH would have little to no effect on increasing blood volume.
" In response to low blood pressure , why does ATII and aldosterone increase H+ secretion and HCO3- reabsorption respectively? " !!
AT II promotes HCO3 - reabsorption in PCT ; while aldosterone promotes H+ secretion in the late DCT & collecting tubules with a net result of CONTRACTION ALKALOSIS !
My humble understanding of the conjunction between the drop in BP & the rise in pH is that it's a kind of compensatory mechanism ; where drop in BP ==> tissue hypoperfusion ==> cellular switch to anaerobic metabolism ==> lactic acidosis ==> elevated AG metabolic acidosis ! So contraction alkalosis helps rapidly mitigate the effects of low pH on the vital organs like CNS & heart !
Lord knows best !
thank you very much mister eric
For your slide @15 min, why is Cushing Syndrome included in causes of mineralocorticoid excess. Isn't Cushing Syndrome an increase of cortisol which is a glucocorticoid?
Although cortisol is classified as a glucocorticoid, it has some mineralocorticoid activity. Here's an article that discusses some of the relevant physiology: www.karger.com/Article/FullText/314315
@@StrongMed Thank you. Lots of great info in this article. I was surprised to learn that cortisol activates the RAAS (something they don't teach us in med school)
@@TheSpades21 I read in that paper dating to 2010 that cortisol enhances (RAAS) despite plasma renin activity and plasma renin concentration are generally normal or suppressed in patients with CS !
Does this make any sense ?
I click on the Subscribe icon but it does not subscribe , I don't understand
Great lecture! Are you considering including treatment options for metabolic alkalosis aswell?
Thanks for your comment. Unfortunately, there are no immediate plans to discuss treatment options here - too many other requested topics... Hopefully, someday I can circle around to the acid-base topics again.
crystal clear lectures
Thank you . Good lecture.
Hi Dr Eric thank you only now I understand ABG will you be taking acute renal failure chronic renal failure I use your lectures for step 3
thanks asha
Asha Krishnaq I'm hoping to cover acute and chronic renal failure in September/October.
One word...Legit!!!
Thanks a great work!!!
I'm carnivore and don't eat carbs at all. ZERO carbs. Recently, I was sick with a virus. Just before, what I thought was full recovery, I became very weak. I suddenly needed sugar. I ate three packets of sugar and a Snickers Bar and soon felt better. When I got home, I ate two bowls of icecream. The next day, I was still a little weak so I had a small bowl of icecream and a prtein shake. Less than an hour later, I was in the Emergency Room. There, I was given three IV bags and two big Potassium pills. I was told that my Potassium was low, which I found strange because I salt my meat with a 50/50 blend of NaCl and Potassium Citrate. I actually had an electrlyte drink that morning. My discharge papers say Accute Respiratory Alkalosis but I can't help but think that it was more due to my etreme insulin sensitivity and my sugar intake. I wasn't haveing diarrhea and only vomited once. Potassium being low makes me think that it wasn't Milk-Alkali Syndrome but all that icecream that I consumed makes me wonder. 3 weeks prior, my Potassium was 4.9.
nice lecture
8:30
excellent
thank you very much
Thanks
U have a spelling mistake in first slide... ALKALOSES
Alkaloses = pleural of alkalosis. en.wiktionary.org/wiki/alkaloses
ممتاز
Thank you Dr Eric using all your lectures for USMLE Step 3 new exam
nobody can teach like you
thanks
thanks