Metabolic acidosis 2 questions

[Danyy361991]

Hi there folks!
After passing through the review books for answers (both BRS and Rapid Review) I have decided to take off the gloves and ask my comrades for help!

I have 2 questions regarding Metabolic acidosis with normal anion gap originating from Diarrhoea.

1. The colon & pancreas secrete actively HCO3- thus when we have diarrhoea we lose this HCO3-(Rapid review): My question is: WHO CARES? this HCO3- is already secreted from the blood, and it is no reabsorbed excessively in the intestine, so why does it even matter that we lose it in the HCO3-? it is not in our blood anyhow.

2. It is written that in the case of Metabolic Acidosis originating in Diarrhoea we compensate by increasing our blood Cl-, my question is how? , I didn't find the mechanism nowhere.

Thanks for the help folks, I truly appreciate it no kidding.

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[dorster]

How i understand it is that metabolic acidosis with diarrhea only happens with severe secretory diarrhea where you're losing an excessive amount of bicarb in the stool. Normal amounts of bicarb in stool won't cause metabolic acidosis, but when it's severe and the patient is constantly losing fluid in the diarrhea the amount of bicarb secreted increases so it becomes a substantial loss and the kidney can't make up for it by reabsorbing more bicarb so thats when they get metabolic acidosis and often hypokalemia. Im not sure the actual mechanism of the increase in chloride but i know that if there is any type of metabolic acidosis that means theres an overall increase in H+ in the blood and in order for electrolytes to stay neutral that means there always has to be an increase in another anion. Its either going to be Cl- or some other hidden anion. If its chloride then thats hyperchloremic metabolic acidosis and its either due to loss of bicarb from the intestines or loss of bicarb from the kidney. If its a hidden anion then that means its high anion gap metabolic acidosis and its due to one of the additional acids (ex: lactic acidosis or methanol).

 

[Danyy361991]

How i understand it is that metabolic acidosis with diarrhea only happens with severe secretory diarrhea where you're losing an excessive amount of bicarb in the stool. Normal amounts of bicarb in stool won't cause metabolic acidosis, but when it's severe and the patient is constantly losing fluid in the diarrhea the amount of bicarb secreted increases so it becomes a substantial loss and the kidney can't make up for it by reabsorbing more bicarb so thats when they get metabolic acidosis and often hypokalemia. Im not sure the actual mechanism of the increase in chloride but i know that if there is any type of metabolic acidosis that means theres an overall increase in H+ in the blood and in order for electrolytes to stay neutral that means there always has to be an increase in another anion. Its either going to be Cl- or some other hidden anion. If its chloride then thats hyperchloremic metabolic acidosis and its either due to loss of bicarb from the intestines or loss of bicarb from the kidney. If its a hidden anion then that means its high anion gap metabolic acidosis and its due to one of the additional acids (ex: lactic acidosis or methanol).

Thanks man, greatly appreciated really.
Where did you learn Acid Base disorders from?

 

[dorster]

i actually have a really awesome book for electrolytes its the "acid base fluids and electrolytes made ridiculously simple" book and its super short so its good if you just need to look something up really fast

 

[soop]

Hi there folks!
After passing through the review books for answers (both BRS and Rapid Review) I have decided to take off the gloves and ask my comrades for help!

I have 2 questions regarding Metabolic acidosis with normal anion gap originating from Diarrhoea.

1. The colon & pancreas secrete actively HCO3- thus when we have diarrhoea we lose this HCO3-(Rapid review): My question is: WHO CARES? this HCO3- is already secreted from the blood, and it is no reabsorbed excessively in the intestine, so why does it even matter that we lose it in the HCO3-? it is not in our blood anyhow.

2. It is written that in the case of Metabolic Acidosis originating in Diarrhoea we compensate by increasing our blood Cl-, my question is how? , I didn't find the mechanism nowhere.

Thanks for the help folks, I truly appreciate it no kidding.

High volume stool flow i.e. diarrhea, has high NaCl concentration. The ileum and colon has ENaC, ROMK channels & HCO3-/Cl- exchangers similar to the ones found in the kidney. Basolateral sodium-potassium ATPase creates an intracellular environment that favors Na+ reabsorption & K+ secretion. This results in hypokalemia seen in diarrhea. Cl- follows Na+ at the expense of bicarb, which results in the non-anion gap acidosis.

 

[Danyy361991]

High volume stool flow i.e. diarrhea, has high NaCl concentration. The ileum and colon has ENaC, ROMK channels & HCO3-/Cl- exchangers similar to the ones found in the kidney. Basolateral sodium-potassium ATPase creates an intracellular environment that favors Na+ reabsorption & K+ secretion. This results in hypokalemia seen in diarrhea. Cl- follows Na+ at the expense of bicarb, which results in the non-anion gap acidosis.

Hi there mate, So I will try to take your explanation and fit it into my brain and you tell me if it is correct:

- In the Colon and Ileum we have Channels that:
1. LET potassium OUT to the gut and reabsorb Na.
2. Kick bicarbonate out of the cell in exchange for Chloride (same as a PCT basolateral membrane antiporter)

Now the question to be asked is:
- Why when a person has Diarrhea he losses more K and HCO3- than usual?

Possible answer: concentration gradient becomes greater as the person losses HCO3- and K in the diarrhea?

The explanation I found in the book (made ridiculously simple) for the Cl- compensation in the anion gap is the following:
because in the diarrhea we have more Na+
than Cl- and both are anionic gap
components even though we have HCO3-
loss, we have an equivalent amount of Na
loss

=)!

 

[soop]

Hi there mate, So I will try to take your explanation and fit it into my brain and you tell me if it is correct:

- In the Colon and Ileum we have Channels that:
1. LET potassium OUT to the gut and reabsorb Na.
2. Kick bicarbonate out of the cell in exchange for Chloride (same as a PCT basolateral membrane antiporter)

Now the question to be asked is:
- Why when a person has Diarrhea he losses more K and HCO3- than usual?

Possible answer: concentration gradient becomes greater as the person losses HCO3- and K in the diarrhea?

The explanation I found in the book (made ridiculously simple) for the Cl- compensation in the anion gap is the following:
because in the diarrhea we have more Na+
than Cl- and both are anionic gap
components even though we have HCO3-
loss, we have an equivalent amount of Na
loss

=)!

In a hypotonic meal, a large portion of the NaCl is absorbed in the proximal small intestines via solvent drag along with the water. Increased GI motility reduces the time the bolus is exposed to the proximal small bowel → colon working overtime.

 

[Danyy361991]

In a hypotonic meal, a large portion of the NaCl is absorbed in the proximal small intestines via solvent drag along with the water. Increased GI motility reduces the time the bolus is exposed to the proximal small bowel → colon working overtime.

I am still not here with you mate, can I have the sources name?

 

[soop]

I am still not here with you mate, can I have the sources name?

Sure thing.

Medical Physiology by Rhoades & Bell. Lower GI electrolyte homeostasis starts on page 530.

Let me see if I can summarize everything.

First, solvent drag is the paracellular transport of ions via bulk flow. When you have a large hypotonic bolus in your stomach, much of the water is reabsorbed paracellularly in between the enterocytes of the proximal portion of the small intestines, i.e. duodenum & jejunum. Small ions like sodium and potassium flows across the same way as a strong current in a river drags debris further downstream. This transport mechanism is responsible for reabsorption of a significant amount of NaCl. Another mechanism of Na+ absorption is coupled via symports such as the SGLT-1 transport or amino acid transports. This also results in paracellular absorption of Cl-.

In the The basolateral surfaces, i.e. the side away from the lumen, have Na+/K+ ATPases which actively transports Na+ out of the enterocyte into the blood stream and transports potassium into the enterocyte. Distal ileum and colon expresses ENaC channels, which facilitates reabsorption of Na+ from the lumen and ROMK channels, which facilitates secretion of K+ into the lumen. In addition, there are HCO3- & Cl- exchangers which allows for the reabsorption of Cl- at the expense of HCO3- loss. These transports are "load dependent" in the sense that if the proximal small bowel reabsorbs most of the NaCl, then the ileum/colon's transporters are not as active. However, in situations of rapid GI motility, the proximal small bowel may not have enough time to reabsorb sufficient NaCl from the bolus before the bolus has passed the the proximal small bowel into the ileum/colon. Now the ileum/colon transports have to work overtime in order to minimize NaCl loss and it will do so at the expense of K+ (via ENaC & ROMK channels here are functionally linked) and bicarb (HCO3-/Cl- exchanger). This results in excess K+ and bicarb loss in diarrhea.

Hope it helped.

 

[Danyy361991]

Sure thing.

Medical Physiology by Rhoades & Bell. Lower GI electrolyte homeostasis starts on page 530.

Let me see if I can summarize everything.

First, solvent drag is the paracellular transport of ions via bulk flow. When you have a large hypotonic bolus in your stomach, much of the water is reabsorbed paracellularly in between the enterocytes of the proximal portion of the small intestines, i.e. duodenum & jejunum. Small ions like sodium and potassium flows across the same way as a strong current in a river drags debris further downstream. This transport mechanism is responsible for reabsorption of a significant amount of NaCl. Another mechanism of Na+ absorption is coupled via symports such as the SGLT-1 transport or amino acid transports. This also results in paracellular absorption of Cl-.

In the The basolateral surfaces, i.e. the side away from the lumen, have Na+/K+ ATPases which actively transports Na+ out of the enterocyte into the blood stream and transports potassium into the enterocyte. Distal ileum and colon expresses ENaC channels, which facilitates reabsorption of Na+ from the lumen and ROMK channels, which facilitates secretion of K+ into the lumen. In addition, there are HCO3- & Cl- exchangers which allows for the reabsorption of Cl- at the expense of HCO3- loss. These transports are "load dependent" in the sense that if the proximal small bowel reabsorbs most of the NaCl, then the ileum/colon's transporters are not as active. However, in situations of rapid GI motility, the proximal small bowel may not have enough time to reabsorb sufficient NaCl from the bolus before the bolus has passed the the proximal small bowel into the ileum/colon. Now the ileum/colon transports have to work overtime in order to minimize NaCl loss and it will do so at the expense of K+ (via ENaC & ROMK channels here are functionally linked) and bicarb (HCO3-/Cl- exchanger). This results in excess K+ and bicarb loss in diarrhea.

Hope it helped.

1st: It helped a l-o-t, we actually got an answer here! I am super happy about it, and even more due to the fact that finally I found a place where I can ask stuff.

2nd:I still couldn't find an explanation about Hypokalemia, why were they connected by now: (pub med)
"but fecal K+ losses are increased in diarrheal diseases by unabsorbed anions (which obligate K+), by electrochemical gradients secondary to active chloride secretion"

3rd: Now to put this note right near the proper paragraph in my RR pathology book.

Thanks!