You, sir, are gold. I honestly though I wouldn't pull through 40 minutos of biochem but you made profoundly enjoyable. Thanks for all the effort you put in this.
thank you Dr Strong , good lecture. oh my god time fly , i listened to this 4 year ago. i wish you good luck and great health to keep makinf educcational video like this.
***** Lactic acidosis secondary to malignancy is best described in hematologic malignancies - leukemia and lymphoma. In my completely anecdotal experience, lymphoma is the more common of the two to do this, and I've seen several patients with lactates chronically > 10mmol/L (normal < ~2mmol/L)
1. Thank you so much for all of your videos - they are priceless. 2. I'm so glad there's another person who hates mnemonics as much as I do. I can't get away from them, no matter how hard I try! Thanks again for another great lecture!
Thank you Doctor Strong. Actually it is a great lecture. I learn new thing that i never heard before. Although i have to watch it a couple time. I thank you for your kindness to provide knowledge to doctors around the world.
This is a super lecture. You went on to cover toxin and easily explain . You use your free time to make a lecture series which i think is the best out there in medical education in youtube world so to speak. After listening couple time of your lecture, it is easier to read Wash U manual . more palatable afterward. I cant thank you enough and wish you luck throut out this covid-19 period.
Hi Eric, I have one question that troubles me and my colleagues in clerkships. I think we are missing some basic chemistry concept but we all can’t manage to figure it out. How does lactate make a patient acidic? As lactate is the conjugate base of lactic acid. I would assume it lost its H+ already. And when pyruvate forms lactate in 5:30, it even takes away an H+ away from the blood when forming NAD+, making the patient more alkalotic? As you say D-lactate can also result in a lactic acidosis I much wonder how. Bonus question: can hyperventilating increase lactate that shows up in the ABG result? As with blowing CO2 away decreases H+ in the blood and if you have an equilibrium reaction: CH 3CH(OH)COO + H+ CH 3CH(OH)COOH taking away the H+ results in less lactate and more lactic acid? Thanks a lot for the amazing videos, they help me a lot in understanding specific topics in more depth.
I was wondering why with bicarb 26 and ph 7.41 we call it metabolic acidosis if bicarb of 26 is high not low. Thx. Also I have a question: is it true that one need to fix metabolic Alkalosis for electrolytes to be able to be appropriately replenished. Thx
first, thanks for these fabulous lectures. second i have a question as a case senario. patient on mechanical ventilator and ABG : PH=7.47,Pco2=31,HCO3=22,Na=152,K=3.7,CL=109,ALB=2.6. when i came to adjusted AG it is 24.5. delta ratio should be calculated as 24.5 minus 12 or measured AG which is 21 minus 12.?
Let's say if we neglected the electrolyte & albumin concentrations without calculating the AG , it would be a case of compensated respiratory alkalosis !But that would seem to be the tip of the iceburg ! The derangement in various electrolyte concentrations is a reflection of the body's attempt to restore its electroneutrality in the course of the ongoing acid-base disorder !
@@WhyNot-si4pj Since pH it’s not normal, actually > 7.45, can I assume that the elevated anion gap is due to a metabolic acidosis like in the video of mixed disorders with normal pH? How could I know here if the elevated anion gap is due to other cause and not due to metabolic acidosis? Because I thought that I can only assume a metabolic acidosis just based on elevated anion gap only is cases where pH is normal. Now being more clear: independent of the pH (normal, acidemic or alkalemic), is it possible assume there is a metabolic acidosis only because of a elevated anion gap? If no, how can I possibly distingue those elevated anion gap with acidosis and those with no acidoses (just elevated anion gaps)? I’m a little confused now, and this is the second phase of the algorithm presented in the final os this present video, so if you could help me please.
@@carmicael6866 The pH is 7.47 , so we can't assume it a normal pH ! The case was heading towards a normal pH , but shifting from the high anion gap metabolic acidosis to metabolic alkalosis resulted in reversal in its respiratory compensation before being admitted to the ICU & put on the ventilator ! The answers to all of your questions are not there in the algorithm sequence ; but rather in the histories , the complete metabolic panels & toxicology screenings of every individual case ! They reflect a lot ; especially in case of altered anion gap with normal pH .
In your discussion of methanol and the utility of the OG, I'm a bit confused as to why formic acid does not cause an elevation in the OG. It seems formic acid would be an osmole and quick research shows osmole measuring instruments use freezing point depression to measure. I would think formic acid would cause a change in freezing point. Does this also apply to other metabolites of toxic alcohols or just formic acid? Thanks in advance for your response and your time in making these videos!
Methanol creates a more osmotic gradient compared to that of formic acid ! The hydroxyl group (OH) of alcohols - like methanol - have higher capacity to establish hydrogen bonds with water molecules than the carboxylic groups (COOH) of acids - like formic acid . As a result , larger number of water molecules bind to methanol compared to those binding to formic acid ! So as long as the methanol concentration in blood is higher than that of formic acid , a higher osmolal gap (OG) is expected !
Lymphomas , leukemias , multiple myeloma , ……. etc .Possibly due to the extra needs of neoplastic cells for oxygen in the course of their rapid growth & proliferation .So that relative shortage of oxygen supply will result in impaired aerobic metabolism in those neoplastic cells & shift towards anaerobic metabolism with subsequent production of LACTIC ACID !
Any significant metabolic derangement in an individual that young suggests the *possibility* of a genetic disease, particularly if common non-genetic causes were ruled out (e.g. lactic acidosis from hypoperfusion, renal failure). I'm not a pediatrician, but I imagine if the anion gap and/or acidosis seemed high enough to be clinically relevant, the child might benefit from a visit to a metabolic specialist. Without knowing more details, possible genetic causes would include an organic acidemia, inborn error of fatty acid or carbohydrate metabolism, or a mitochondrial disorder.
You, sir, are gold. I honestly though I wouldn't pull through 40 minutos of biochem but you made profoundly enjoyable. Thanks for all the effort you put in this.
thank you Dr Strong , good lecture.
oh my god time fly , i listened to this 4 year ago.
i wish you good luck and great health to keep makinf educcational video like this.
I think this the best lecture in the universe about metabolic acidosis ..
Words of appreciation are not enough to describe my gratitude for your dedicated high quality work. Thank you Sir
***** Lactic acidosis secondary to malignancy is best described in hematologic malignancies - leukemia and lymphoma. In my completely anecdotal experience, lymphoma is the more common of the two to do this, and I've seen several patients with lactates chronically > 10mmol/L (normal < ~2mmol/L)
1. Thank you so much for all of your videos - they are priceless. 2. I'm so glad there's another person who hates mnemonics as much as I do. I can't get away from them, no matter how hard I try! Thanks again for another great lecture!
Thank you Doctor Strong. Actually it is a great lecture. I learn new thing that i never heard before. Although i have to watch it a couple time. I thank you for your kindness to provide knowledge to doctors around the world.
This is a super lecture. You went on to cover toxin and easily explain . You use your free time to make a lecture series which i think is the best out there in medical education in youtube world so to speak. After listening couple time of your lecture, it is easier to read Wash U manual . more palatable afterward. I cant thank you enough and wish you luck throut out this covid-19 period.
This is a bloody brilliant lecture :)
YOU CHANGED MY LIFE
absolutely amazing. I learned so much! Thank you!!
You are the best!!! Love all of your lectures!!!! THANK YOU!!!
I love you for making this lecture video!....
excellent teacher, greetings from Colombia
Hi Eric, I have one question that troubles me and my colleagues in clerkships. I think we are missing some basic chemistry concept but we all can’t manage to figure it out. How does lactate make a patient acidic?
As lactate is the conjugate base of lactic acid. I would assume it lost its H+ already. And when pyruvate forms lactate in 5:30, it even takes away an H+ away from the blood when forming NAD+, making the patient more alkalotic? As you say D-lactate can also result in a lactic acidosis I much wonder how. Bonus question: can hyperventilating increase lactate that shows up in the ABG result? As with blowing CO2 away decreases H+ in the blood and if you have an equilibrium reaction: CH 3CH(OH)COO + H+ CH 3CH(OH)COOH taking away the H+ results in less lactate and more lactic acid? Thanks a lot for the amazing videos, they help me a lot in understanding specific topics in more depth.
I was wondering why with bicarb 26 and ph 7.41 we call it metabolic acidosis if bicarb of 26 is high not low. Thx. Also I have a question: is it true that one need to fix metabolic Alkalosis for electrolytes to be able to be appropriately replenished. Thx
Wonderful lecture 👌👌👌👌👌
Profound thanks for these awesome lectures
Thank you so very much Sir
You are a god amongst humans
first, thanks for these fabulous lectures. second i have a question as a case senario. patient on mechanical ventilator and ABG :
PH=7.47,Pco2=31,HCO3=22,Na=152,K=3.7,CL=109,ALB=2.6. when i came to adjusted AG it is 24.5. delta ratio should be calculated as 24.5 minus 12 or measured AG which is 21 minus 12.?
Did U found the answer plz?
It's of course the adjusted AG - 12 , i.e : 24.5 - 12 !Measured AG = Na - (HCO3 + Cl) = 152 - (22+109) = 152 - 131 = 21 .Adjusted AG = Measured AG + 2.5 (4 - serum albumin) = 21 + 2.5 (4 - 2.6) = 21 + 3.5 = 24.5 . Delta ratio = 24.5 - 12 / 24 -22 = 12 .5 / 2 = 6.25 . Elevated anion gap metabolic acidosis + metabolic alkalosis + respiratory alkalosis =====>>> Triple acid - base disorder .The clinical scenario will help us figure out the etiology of the disorder , BUT adjusting the mechanical ventilator's pressures will help correct the respiratory alkalosis .
Let's say if we neglected the electrolyte & albumin concentrations without calculating the AG , it would be a case of compensated respiratory alkalosis !But that would seem to be the tip of the iceburg ! The derangement in various electrolyte concentrations is a reflection of the body's attempt to restore its electroneutrality in the course of the ongoing acid-base disorder !
@@WhyNot-si4pj Since pH it’s not normal, actually > 7.45, can I assume that the elevated anion gap is due to a metabolic acidosis like in the video of mixed disorders with normal pH? How could I know here if the elevated anion gap is due to other cause and not due to metabolic acidosis? Because I thought that I can only assume a metabolic acidosis just based on elevated anion gap only is cases where pH is normal. Now being more clear: independent of the pH (normal, acidemic or alkalemic), is it possible assume there is a metabolic acidosis only because of a elevated anion gap? If no, how can I possibly distingue those elevated anion gap with acidosis and those with no acidoses (just elevated anion gaps)? I’m a little confused now, and this is the second phase of the algorithm presented in the final os this present video, so if you could help me please.
@@carmicael6866 The pH is 7.47 , so we can't assume it a normal pH ! The case was heading towards a normal pH , but shifting from the high anion gap metabolic acidosis to metabolic alkalosis resulted in reversal in its respiratory compensation before being admitted to the ICU & put on the ventilator ! The answers to all of your questions are not there in the algorithm sequence ; but rather in the histories , the complete metabolic panels & toxicology screenings of every individual case ! They reflect a lot ; especially in case of altered anion gap with normal pH .
Excellent 👏👏
In your discussion of methanol and the utility of the OG, I'm a bit confused as to why formic acid does not cause an elevation in the OG. It seems formic acid would be an osmole and quick research shows osmole measuring instruments use freezing point depression to measure. I would think formic acid would cause a change in freezing point. Does this also apply to other metabolites of toxic alcohols or just formic acid? Thanks in advance for your response and your time in making these videos!
Methanol creates a more osmotic gradient compared to that of formic acid ! The hydroxyl group (OH) of alcohols - like methanol - have higher capacity to establish hydrogen bonds with water molecules than the carboxylic groups (COOH) of acids - like formic acid . As a result , larger number of water molecules bind to methanol compared to those binding to formic acid ! So as long as the methanol concentration in blood is higher than that of formic acid , a higher osmolal gap (OG) is expected !
Thank you very much
Thank you very much!
Thnx a million
10 years later... have the questions on metformin been answered?
In extreme brief...no. ¯\_(ツ)_/¯
Nice speech in metabolic acid
Thank you dear teacher !
Does these lectures has short notes or slides ?
I'm sorry, they do not.
Is there a recommended book to follow you with it?
Could you give some examples of tumors that produce lactate?
Lymphomas , leukemias , multiple myeloma , ……. etc .Possibly due to the extra needs of neoplastic cells for oxygen in the course of their rapid growth & proliferation .So that relative shortage of oxygen supply will result in impaired aerobic metabolism in those neoplastic cells & shift towards anaerobic metabolism with subsequent production of LACTIC ACID !
Hi sir my son eliveted lactic acidosis, (lEM) what is the treatment sir please tell me, age(2year)
I'm very sorry, but I cannot give specific, individualized medical advice here. I recommend speaking with your son's pediatrician.
This problem what is the feutcher sir tell me about the elivated lactatic acid IEM
Thanks
Great lecture, as always. But why do you hate mnemonics? They are so usefull! hahaha
If an anion gap level is to high what does that mean in a 9 week infant
Any significant metabolic derangement in an individual that young suggests the *possibility* of a genetic disease, particularly if common non-genetic causes were ruled out (e.g. lactic acidosis from hypoperfusion, renal failure). I'm not a pediatrician, but I imagine if the anion gap and/or acidosis seemed high enough to be clinically relevant, the child might benefit from a visit to a metabolic specialist. Without knowing more details, possible genetic causes would include an organic acidemia, inborn error of fatty acid or carbohydrate metabolism, or a mitochondrial disorder.
😊
2024 anyone?
Still here making videos!
KULT
GOLDMAIT
metformin info at 8:30