Electrolytes

hello in this lecture we will investigate electrolyte balance you have already studied many of these electrolytes between bio19 and bio 203 in fact this table is from your bio19 book and so I'm sure you recognize these major electrolytes in the human body when we study electrolytes they have many important fun functions and as you read through the functions you'll see they help with uh resting membrane potentials action potentials which have that depolarization repolarization we need them for al

l muscle contraction and nerve impulses all those excitable cells some are really important for fluid balance we know that calcium has multiple functions in the body and so as we go through the electrolytes we're going to focus on the ones in this table the sodium pottassium calcium magnesium and chloride and we know that we take them in through what we eat and drink drink we lose them through urine and feces we lose a little bit of salt that way we also lose salt when we sweat perspiration has

sweat and we lose even more if we were to have a GI disorder such as vomiting or diarrhea and the kidneys are really important in monitoring and maintaining our electrolyte balance because our kidneys can to some extent control the amount of the electrolyte that's either reabsorbed back into the blood or secreted to excess the body and urine we're going to start with sodium you do not need to memorize the normal value so what I would like you to do is know the electrolyte know the main functions

of the electrolyte and then we'll also look at factors that affect it in our blood such as usually hormones so when we look at sodium we know that in fact we probably get too much sodium in our diet more than anything else so we gain it through what we eat uh you can see see a lot of our in our table salt that we add to Foods so typically we take in too much salt we lose a little bit of sodium in our urine and as I mentioned we can also lose it through sweat the main hormones that control sodiu

m balance are aldosterone and Angiotensin 2 is here because remember Angiotensin 2 once it's formed will be a trigger to release aldosterone and so aldosterone's critical because it really controls that sodium reabsorption in the DCT the um sodium reabsorption remember is talking about the sodium leaving the filtrate and going back into the blood you might remember that Angiotensin 2 in addition to triggering the release Al of aldosterone can also impact sodium reabsorption but in the PCT now mo

st sodium is reabsorbed in the PCT we said roughly 75% of it but if you have aldosterone that's when we get the rest of that sodium in our DCT so if we're looking at the triggers for aldosterone or Angiotensin 2 one thing that's going to trigger it is going to be anytime our plasma sodium levels fall because if our sodium levels were to decrease then that's going to be a signal that we need to raise them again and so that's one of the factors we also know that these are released anytime there's

a decrease in blood volume or a decrease in blood pressure now Addison's disease is something you learned in amp1 and when we look at Addison's disease this is hypo aldosteronism you might remember that endocrine disorders can be hyper or hypo so the aldosterone comes from the adrenal cortex and in this disease it's not making this hormone and so what can happen if you don't have enough aldosterone is that you're going to end up losing sodium in your urine and water will follow it so you're goin

g to have low blood pressure you're probably going to feel weak for some reason it can cause a change to the skin it causes a bronzing of the skin and I'm not sure why but um Addison disease occurs from that now ANF is the antagonistic hormone to aldosterone you can also call this& what you want to call atrial ntic peptide or factor this comes from the Atria of the heart and notice it's both a diuretic and a naturetic now you know a diuretic is something that's going to increase urine output so

it's going to cause us to lose more water in our p and it's a naturetic because it increases the secretion of sodium so when ANF is released it actually will cause your kidneys to kick out the sodium so you're decreasing sodium reabsorption which means it's leaving in the urine and water tends to follow and so it's going to increase your urine output that would lower your blood volume and lower your blood pressure so things that typically stimulate its release would be anytime we had a high plas

ma sodium level or theoretically we had a higher blood volume or higher blood pressure and of course we have hypertension in this country and so we know that it's not just due to the blood volume that's causing the hypertension or we would never have it because A&P would take care of that um typically remember it's due to maybe atherosclerosis or blood vessels that aren't quite as flexible some other hormones that affect sodium levels are estrogen and progesterone estrogen tends to hold on to so

dium so it increases sodium and even chloride reabsorption and estrogen is going to rise right before your menes and so this might be why you retain water you might get a little swollen adem before your menes whereas progesterone is released after your menstrual cycle has passed and that works as a diuretic and it helps remove all that water if we have too much or too little sodium we can have hyper nmia which is too much and hypo which is too little whenever we have too much it could actually m

ake our cells even more excitable because remember that sodium entering the cell is the first step to depolarize any electrically excitable cell so these cells could become more excitable if we have high sodium levels we're basically dehydrated if we have too much sodium then we have more solutes so we're probably going to feel thirsty maybe be a little lethargic hybon atmia is not having enough sodium this could be if your blood's very very dilute if you have too much water intake we looked at

this with hypotonic hydration um it could be some medications or excessive alcohol intake and now we're going to have more muscle weakness and cramps because now we're not able to depolarize those cells when we're looking at this disruption in sodium if we're looking at hyper we looked at the fact that if we increase sodium then our plasma osmolarity is going to be too high the blood's too salty and when that happens remember that's a trigger for 0 so I just wanted to bring ADH back as a reminde

r when we studied this with the urinary system and then the ADH is going to open those aquaporins and try to hold the water to correct the hypernia if we have hyponatremia we have more dilute blood now we're going to inhibit ADH we don't open the aquaporin and so now we excrete a lot of water we have a large urine output and I had mentioned that it takes about 45 minutes to inhibit ADH and so if you are drinking a lot of water or watery beer or alcohol you'll notice it takes roughly 45 minutes b

efore you start having to urinate more our other important um cation is potassium we know that potassium is the main one in our ICF and it's critical for normal cell functioning we need it specifically for that resting membrane potential we need it for our neurons and our muscles to function so we can say neuromuscular function when we look at potassium again we know that most of it is inside the cell and that created that diffusion gradient because there's more potassium inside and less outside

potassium wants to leave the cell in fact it did leave the cell through those leak channels which is why our rmp was negative so anything that disrupts our extracellular potassium concentration can affect this diffusion gradient and the resting membrane potential you might also remember that once you got an action potential you had your depolarization and then you had your repolarization when it resets and that repolarization was due to pottassium leaving the cell so we could also have some con

cerns with the repolarization when we look at pottassium we do try to make sure we take in as much as we lose but when we're looking at it one of the things with potassium is we lose it every single day in our urine so we will always lose potassium in our urine which is why it's important to make sure you're taking it in every day we do know the kidneys can adapt if the potassium concentration in the ECF goes up if there's more in your blood then the renal tubules will actually secrete even more

to get rid of it but notice they can't hold on to it if it should fall we also know that it's critical when we look at the pH of the extra cellular fluid and we know that there's this relationship between pH and potassium remember that if we should have a pH decreases that means that you have too many hydrogen ions so now you're going to want to get rid of the hydrogen ions so you would increase the hydrogen ion secretion well potassium and hydrogen compete for secretion so if I'm increasing my

hydrogen secretion I'm kicking that out into my P now I'm going to decrease my pottassium secretion and in fact pottassium levels could go up in my blood I could have hyperemia from that on the other hand if my pH should go up if my pH increases that's because I don't have enough hydrogen ions so now I don't want to get rid of them so in this situation I would decrease my hydrogen ion secretion I need to hold on to them but something's got to go so now I'm going to increase pottassium secretion

so more potassium leaves which could send me into hypoc calamia and as I mentioned we lose potassium every single day and this is mainly due to aldosterone aldosterone definitely affects sodium however it's a one toone pump so for every sodium that comes back one potassium has to leave and so we release aldosterone every day because we reabsorb most sodium from our urine which means that every day we will we will lose potassium in our urine it's estimated to be about 10% so again eat a banana m

ake sure you're getting foods that have potassium so you can replenish that if our potassium levels go up that would stimulate aldosterone because aldosterone's job is to lower them so if we're looking at hyper or hypo calmia we're coming back and we're looking at those cells now hyperemia remember would be commonly seen if you had kidney failure because the kidneys aren't getting rid of that extra pottassium and so if we come back to our cell now we know we have a lot of potassium inside but wh

at now if I have more outside what's going to happen to that diffusion G will potassium want to leave and the answer is no it's not going to want to leave so now it's going to stay inside the cell so where we had our normal negative rmp and then we always had this threshold level well now potassium staying inside so my resting membrane potential is going to creep toward threshold my cells are going to get much more excitable because we're getting closer and closer to threshold it's easier to exc

ite them and depolarize them often you have a tall spiked t-wave as well on an EKG and you could see it that way and then as well you know once we have this pottassium and outside of the cell this could also interfere with the repolarization stage so at first the cells get really excitable but then if this goes on longer they actually can't they kind of like run out of steam so to speak they're no longer excitable and so then they actually become inhibit inhibited now hypokalemia on the other ha

nd we're looking at too low potassium and this could happen from diuretics because every time we urinate we lose potassium from our body this could also happen if we had an issue with aldosteronism having too much of it released notice hypo causes a small t-wave and it can cause what's called a uwave which is this little u-shaped depression now if we go back to our cell again and now if I really shrink that potassium outside of the cell now potassium really wants to leave and if we lose more pot

tassium remember that is going to hyperpolarize the cell it's going to make it more negative which is going to be inhibitory so you're going to have more muscle weakness remember that pottassium hyper and hypo definitely affect your heart they both can cause fatal arrhythmias and even cardiac arrest other factors that affect potassium so we mentioned aldosterone will lower potassium levels in your blood because it's making you urinate out I would like you to know that cell damage often increases

plasma levels because cells have so much potassium when the cells die they rupture and all that potassium goes into your into your interstitial fluid and your blood we already mentioned how acidosis could increase it because remember in acidosis you're going to your kidneys will get rid of the hydrogen and hold on to the potassium you don't really have to worry too much about these medications but I would like you to recognize insulin so you'll be giving patients insulin and just understand tha

t when you give insulin it causes a reaction with pottassium it actually helps pull potassium into the cell so when you give insulin often the plasma potassium level will fall calcium calcium is the most abundant mineral in the body about 99% of all the calcium is found in the skeleton in your bones we know calcium is critical for several functions in fact if you just want the summary view of the importance of all of these just go right back to the table at the very beginning of this lecture we

know we need it for bone density or strength of our teeth it's critical for muscle contraction it removed the TT complex so muscles would contract it's critical for blood clotting and we need it to release all those neurotransmitters they won't be released at the synopse unless calcium enters excuse me so it's controlled by two hormones pth and calcitonin pth is released from the parathyroid glands these are glands on the back of the thyroid gland and so pth is going to be released anytime our b

lood calcium levels ball so if you're not getting calcium in your diet that's an emergency muscle can't contract without calcium this goes for skeletal muscle smooth muscle and cardiac muscle because they all had that TT complex which prevented contraction from occurring it prevented mein from grabbing actin when our calcium levels fall pth has a three-fold approach number one it's going to go to the Bone activate the Osteo class to pull calcium out of the bone and put it into your blood it can

go to the small intestine and increase the calci absorption from food and it can go to the kidney and it can basically help your kidneys hold on to calcium so it would increase the reabsorption remember reabsorption is from the filtrate back into the blood calcitonin is the antagonistic hormone released by the thyroid gland so calcitonin trigger for release is anytime your calci levels go up so you're eating well you're taking in like lots of calcium calcitonin is released it mainly stimulates t

he osteoblast and deposits calcium into your bones it can also increase the secretion of calcium by the kidneys um by the nefron so that you could eliminate more calcium in your urine now if you're prone to kidney stones you don't want to have a high calcium diet because when you're eliminating more calcium in your urine and if you're not staying hydrated if your urine is more concentrated especially with calcium you're more likely to form a kidney stone if we look at hyper and hypocalcemia Hype

r calcemia um probably not going to see that as much as hypocalcemia but if we're looking at hyper calcemia you can see some of this common signs and symptoms and you might wonder why it decreases the on excitability it decreases concentration it can cause muscle weakness because I just told you it makes muscle contract well there's a little complicated interaction going on here we know that we had those voltage gated sodium channels and that sodium is going to enter that cell to depolarize it t

hat was pretty important when we were looking at contraction well what calcium does is it kind of controls these channels it kind of hangs out the channel and it controls how easily it opens so if we have a lot of calcium then what happens is this sodium Channel won't open very well which means that sodium can't come in and it can't depolarize and excite that cell now if we were to have the opposite occur so here's another cell this will be my little sodium Channel and then I'll put my calcium i

f we have hypo calcemia now there's less calcium blocking that channel so now sodium can get in even faster so it's more excitatory if you have hypocalcemia you're more likely to have muscle spasms and muscle cramps if you don't have enough calcium in your diet and so what happens is you can get you don't need to memorize these signs but what can happen is you can have this like um contraction that happens in like your hands and your wrists and so they're just things that you'll see these spasms

kind occur when we have calcium imbalances magnesium we're not saying a lot about it just know most of it is actually in your bone and inside of cells in the ICF it does help form bone structure it's a co-actor for enzymes over 300 enzymes require magnesium and we also know that magnesium can be inhibitory um to calcium so magnesium can actually prevent calcium from entering the cells so if you give magnes iium you could actually increase the calcium levels we also know that higher magnesium le

vels can be um basically they can be inhibitory on neurons and they've been found to relax muscle so for my son when he started having well when he had the epilepsy we put him on magnesium and he still takes magnesium because now he gets migraines and the neurologists have recognized that and we give him magnesium every single day there's some evidence that people of higher magnesium intakes have a lower risk of heart attack because it seems to relax the smooth muscle as well if we're looking at

too high or too low we're not getting too concerned about this but notice you can have hyper hypo hyper magnesia is more depressant I mentioned that it can suppress um muscle contraction and the Brain at really high levels whereas hypom magnesium is by the way usually due to Mal nutrition not taking in a proper diet can cause this and this can cause cramps and hypertension the chloride ions all we're going to say about chloride is it likes to follow sodium everywhere so sodium and chloride are

BFFs we also know that chloride is really important because it is critical for allowing us to transport carbon dioxide and forming that bicarbonate ion and remember that the chloride and the bicarb went in opposite directions and we call that the chloride shift we're not worrying too much about abnormal chloride levels this is more an FYI picture for you because you're not going to see a whole lot of issues with chloride um it mainly will affect uh basically fluid balance so this concludes our l

ecture on electrolytes