Advanced Pathophysiology

Electrolyte Imbalance

So we've talked about regulation of fluids, the distribution of the fluids. We talked about regulation imbalances like edema and hyper, hypotonic situations. Now, we're going to talk about the electrolytes. When we look at the electrolytes, first thing you need to do is look at electro and think they're charged like electrical. Here you have the sodium which has a positive, potassium with the positive, calcium with a double positive, hydrogen with a positive. [inaudible 00:00:23] who loss an electron and they have a slightly positive charge, actually a positive charge like this. We call them cations.

When I see the word cation, I always think of a plus in the middle where the T's at. The anions, chloride, this one's a little more tricky. It's bicarbonate and then phosphate. These are anions, they have a negative charge. So, if you remember, cations have the plus and the others have to be anions. And then there's some other things we'll talk about that are technically non-electrolytes, because they either don't have a charge or they're slightly polar, kind of like water. H2O is not technically charged. It's slightly polar. Proteins typically are slightly polar. Sometimes you'll hear them having a charge like a negative charge. But we'll talk about these and what they can do to electrolytes too.

So, the first thing to think about is the comparison of the intracellular and extracellular fluids. So, when you're looking at the cations, especially things like sodium and potassium, look at where they're at, you have to make sure that you're paying attention to where the balances are. If you had physiology with me, I always push this lame little thing to put in your head, but a cell is like an island surrounded by salt water. So, when you're sitting on the island, you're looking at the salt water, what is salt? I mean, salt is sodium and chloride. So, all that water that surrounds your little island is sodium chloride.

So, in the extracellular fluid around your little island cell, you have lots of sodium and lots of chloride. On this island that you're on, it's just covered with banana trees and why do I say banana? Because you think potassium, right? So, inside the cell, the intracellular fluid is going to be really high in potassium. This chart's really handy, because it will break down each of these for you. Like sodium, you can see the extracellular fluid, lots and lots, but inside of the cell, barely anything.

Potassium, the intracellular fluid is really, really high, but the extracellular fluid's very low. You can go all the way through. So, when you look at some of the chemicals that are inside or the electrolytes are inside of a cell, you've got potassium, you've got a lot of magnesium, you've got a lot of phosphates. Those are really high inside the cell. When you look outside the cell, you can see really high sodium, really high chloride, and then a lot of bicarbonate too comparatively. So, just as an example or a review chart there.

So, you want to remember a couple things. That the body's fluids stay electrically neutral where at in the body can shift between the cells and the extracellular fluid. So, remember, things like neurons and muscles actually use a charge different across the membranes. But overall, your body also maintains osmotically balanced fluids. Some of the terms that we're going to use, molecular weight, when we use this, it's just talking about how heavy the particle is. You've seen these two in the last video. The milliequivalents, we're going to use usually when we're measuring the volume of an electrolyte in your plasma. And then milliosmoles, we'll also use that to talk about osmolarity.

So, when we talk about things like sodium, we'll talk about how your milliequivalents of sodium should be about 140. And then we'll talk about the balance or osmolarity of the fluids is typically around what number, which you already know. Most of fluids in your body are right around 300 milliosmoles. So, when we talk about milliequivalents, usually it's identifying one electrolyte. Where milliosmoles is usually talking about the osmolarity collectively.

The first electrolyte, sodium. You probably remember all the purposes of sodium, but what I'm going to do is each of these electrolytes, I'm going to remind you of the physiology and then kind of ask you or pull out of you, "How do you get these things in your body?" So, what would cause a deficit? Maybe not bring the electrolyte into the body or what organ usually clears electrolytes?

The kidney. So, what would probably happen in an imbalance? Maybe the kidney's getting rid of too much or can't get rid of too much. So, first, I'm going to talk about sodium. Sodium, remember, the primary extracellular fluid cation, because it has what charge over it? Positive. You'd like to maintain right around 140 milliequivalents, so 136 to 145 is the safe range. If it goes under, what would you call it? Would you call it hyper, hypo, or iso? Yup, so you would call it hypo. It's too low. And then you would say, N-A-T, nat and then remia.

So, hyponatremia means low salt in the blood or sodium in the blood. And then over here you would have hypernatremia. Remember, the -emia at the end is referring to the blood. So, it tells you first, how much the particle hypo or hyper, then it says nat for sodium. I always think in NA+ for the nat then -emia in the blood.

Physiological roles of sodium, remember, probably when you took your physiology, we beat you to death with sodium and the action potential. So, sodium, when you're thinking about neurons, sodium goes in and creates an action potential by doing what to an action potential? Does it hyper-polar? Does it de-polar? Does it re-polar? It depolarizes. It actually starts the electrical activity down the action potential. So, sodium is really important for triggering it. The reason I'm pointing these out is because when you look at hypernatremia, too much sodium, what do you think's going to happen? You think you're going to decrease the depolarization or increase it?

So, now you have more sodium in the environment, that sodium wants to race into the cellular faster, you're going to depolarize more frequently. So, what would you expect to happen to neurons in a hyperpolar situation? Would they fire more frequently or less frequently? Do it fire more frequently?

So, when you look at the pathophysiology, as long as you understand this physiology, what's going on over here, you can actually break it. You can say, "Hey, I've got too much of this or too little of this." You can predict what's going to happen and they tell you the symptoms. You'll see as we go through this. I'll spend a little more time on sodium and I'll move a bit quicker in the other electrolytes, because I'm really pushing that you open your mind during this and think about what are the possibilities.

So, the physiological roles with sodium, it helps maintain osmotic balance. Remember, sodium, glucose, proteins are some of the things that really pull water. So, when you see a lot of sodium, it's going to pull a lot of water too. Nerve conduction, muscular function, remember, the membrane of the outside of the muscles is the same way. It's stimulated by sodium. It has an action potential. It'll help regulate acid and base balance.

So, I'm going to walk right through these. First, remember the actions. So, here, you know that sodium is responsible for the action potential propagating down the axon. You also know that it's responsible for the action potential with the neuromuscular junction. So, here, you have the membrane of the muscle, the action potential shoots along, goes down in and allows that muscle to fire. But you also have to think about with cardiac muscle, sodium racing in on cardiac muscle, remember, causes depolarization too. So, those are important physiological functions.

So, again, if you have an increase in sodium, what would you expect to happen to the frequency of depolarization? So, lots and lots of sodium here, very little sodium here, you raise the sodium even more out here, still very little here. What's going to happen to the rate of diffusion and as soon as you open these membranes? It's going to go faster, right? So, it goes faster. What would you expect to happen to the neuron firing? More frequently or more intense firing. So, it's going to have more frequent firing, which you expect things like maybe your ability, kind of anxious feeling. You might expect at a muscle more contractions, more forceful contractions, more frequent contractions, maybe some tetany.

So, those are things you'd expect with too much sodium in your extracellular fluid. It's going to race into the cells faster, maybe a little more forceful contraction of the heart or frequency of the heart. I shouldn't say contraction, because that's actually calcium, but more frequent contraction of the heart, more faster heartbeats, right? So, those are just some ideas to think about.

So, now, let's talk about how you regulate sodium. So, sodium is regulated by aldosterone. But don't forget, why aldosterone is released? It's released if you have low sodium, because it's going to try and pull the sodium back in, but it's also released because your blood pressure drops. So, aldosterone will regulate sodium, but there's more than one cause for it to be released. So, you just have to keep in mind when aldosterone changes, your sodium is going to change with it. And then don't forget those other chemicals like atrial natriuretic peptide or atrio natriuretic hormone.

I know your books use the word ANH before. But just the opposite of aldosterone, what does ANP do to sodium? It makes you lose it. So, if you had a disorder that you released way too much ANP, what would you expect to happen to your sodium levels in your blood? They would drop. If you had a disorder where you could not release ANP, what would you probably predict about the sodium models? They probably go up. So, you can predict what's going on.

Another thing about aldosterone that you can't forget that sodium is not the only chemical regulated by aldosterone. It's also controlled by potassium. Well, let's walk through this pump again. Remember, aldosterone turns on this pump and it pulls sodium into your blood, but at the same time, it kicks potassium out. So, why would potassium turn on aldosterone? Well, if you had really high potassium here in the blood, it would turn on aldosterone to kick the potassium out. Potassium flow into the nephron and then flow out of the body.

So, as you have high potassium, you're kicking out the potassium because of aldosterone, what's happening to your sodium levels at the same time? Those are raising. So, you might see an outcome of hyperkalemia, so too much potassium. Turning on aldosterone, dropping your hyperkalemia down to normal levels, but what would rise at the same time? Sodium. So, you might see hypernatremia as an outcome of hyperkalemia. So, you just have to keep in mind, this is a domino effect. One structure affects another and another. One chemical can affect more than one ion.

All right, so let's do some application. What are the two types of hyponatremia? Well, think about it. If you have a liter of fluid and you have salt in it, if I don't change the number of particles of salt, is it possible that I can change the concentration of salt? Yeah, you don't have to change the number of particles to change the concentration. There are two totally different concepts. Let's say you have a million particles of salt… By the way, your normal serum sodium room is supposed to be 136 to 145. So, in this situation, we've actually dropped the low 135. We've gone down to… How can we do that? Well, we can either lose the salt. So, think about the causes. If you have less salt than normal, what could be the cause? Where do you get salt from? Diet, maybe you're not taking enough salt in?

How do you lose salt? Primarily through the kidney or through sweating. So, you could be doing excessive sweating. You could be losing lots of it through the kidney. Okay, maybe aldosterone is not working. So, those are some possible causes. You want to think about either you're not getting sodium in or you're losing sodium too fast. Sodium is the problem. It's a little bit different than dilutional.

Dilutional is saying that water is actually the issue. Maybe you're putting in way too much water. Your number of sodium particles is the same, but now the concentration of sodium drops. So, things like kidney failure might cause that. It was kidney failure if you're not urinating, you're retaining more and more water. Even through metabolism, remember you're making the water. You're drinking more water. And then what happens is you dilute all the solutes. So, it looks like you have hyponatremia, but in this situation, it's because of water.

So, when you look at this, kidneys are the kind of primary target with dilutional. So, maybe you have something called SIADH. It's called Symptom of Inappropriate ADH. You release too much ADH. What does ADH do? It's an anti-diuretic, which means you retain water. You keep water and it dilutes your salt. So, SIADH. It could be oliguric renal failure.

Oliguric means decreased kidney function, decreased urine output basically. So, you're retaining more water. It can be things like severe congestive heart failure. You're not pumping blood to the kidney, so the kidney can't get rid of that extra water. All these you can see revolve around kidney issues, SIADH working on the kidney, the kidneys slowing down urine output or less blood getting to the kidney. Another problem could be excessive sweating, but it's not the sweating that caused the problem, because when you sweat, you lose electrolytes and you lose water. It's isotonic.

The problem is when people do a lot of sweating, they get really thirsty and usually go for that bottle of Evian. They put pure water back in them, but what's the problem? They lost electrolytes now they're putting pure water in. So, you have to think of that. That's dilutional. And then here, hyperglycemia. This is kind of a tricky one. But with hyperglycemia, you're putting more sugar in the blood.

What's going to happen is that sugar in the blood is going to do what? Remember, sugar, salt and proteins do what with water? They all pour it. So, when you have too much water in the blood, it's because of the sugar. But proportionally, it looks like you have low salt because you have too much sugar and too much water. So, you can see how these situations can be kind of tricky when you're using the terminology. So, of course, who's at risk with the hyperglycemic situations? I'm hoping you're thinking diabetics, right? And then we already talked about water intoxication. Technically, you look it up.

So, dilutional, one of the symptoms or signs you're going to see is this, you're going to have hypervolemia, too much water, hyponatremia but with depletion or what you find is that when there's less salt, there's usually less water. So, here you see usually hypovolemic symptoms. So, decreased blood plasma. You can think of this with the pathway in the cells. If you have less salt in the blood and more water, that's a what type of situation? It's a hypotonic situation. Where's that water going? Is the water going into the cells, or is the water going into the blood? Remember, with hypotonic, the water's moving from the blood out here and going into the cells. It's being sucked in, so you're losing blood volume. So, just kind of think about the pathways when you're looking at these.

Alright, so other clinical manifestations of hyponatremia. I kind of already talked about this. When you think neurons, with hyponatremia, decreased sodium, you need sodium to cause this action potential, remember? So, if you have less sodium, what would you expect to the frequency of action potentials? They would decrease. How would you feel if your neurons fired less? You probably feel tired, sleepy, might have headaches, confused about where you're at. We'll talk about these things when we talk about the nervous system too. Your hypothalamus starts shutting down. Your temperature starts dropping, depressed reflexes, and then you start seizing, going to coma. If it's not corrected, you could die.

So, think of the pathway and I just explained the pathway, right? You think about muscles, they get cramps and weakness and fatigue. Remember, you need sodium to go and to fire these muscles too. So, usually, you see these with skeletal muscles, tight? There's gastrointestinal symptoms, nausea, vomiting, it's affecting the medulla oblongata, cramping, some diarrhea. The diarrhea, this is kind of tricky. Because with diarrhea, this can actually be a cause, right? You're losing the sodium.

So, the sodium can't get into your blood, causing hyponatremia. So, it's an interesting concept with the GI tract. But again, when we talked about the organs or the systems that help regulate fluids and electrolytes, just go back and think about them. So, how is it possible that what's going on with the central nervous system? What's going on with the skeletal system? What's going on in the GI

tract? You can think about what's going on with the antagonist system too, right?

So, the first question in this set, so question number six all together, is what are some hypernatremia alterations? So, when you think of it, I just explained hypo and I want you to either look up on the internet, you can look up on your book, I don't care. But in hypernatremia, what would you expect the serum sodium level to be? What number? So, how many milliequivalents? Okay, what system could have caused hypernatremia? Of course, you want to think about bringing in salt, putting out salt, right?

I feel like I'm giving away the answers, but I really want you to do a little bit of the footwork and figure these out. What happens to the sodium level and the water level of the plasma? So, when you have hypernatremia, what would happen to the salts? You've already figured that out back here. What's going to happen to the water's result? So, what would happen to the cells is what you want to think too, right? Why would it give you hypo or hypervolemic symptoms? So, I'm not giving away which of these is going to cause, but I want you to figure out will they have hypovolemic or hypervolemic symptoms? What's actually doing that? So, think about the cells and how it's affecting the [inaudible 00:17:25].

And then, I kind of slipped in, put some things in here. Here's some other symptoms you could expect. So, intercellular dehydration, some convulsions, pulmonary edema. So, when you think about hypernatremia, why would it cause convulsions? So, convulsions are typically caused by over firing of neurons, right. So, why would that happen? Pause it and then come back when you're done.

So, just a brief overview and this is kind of a nice little review slide. It has a little extra information that you might want to look into. So, here you have hypernatremia. The problem hypernatremia is that either you have too much salt or too little water. Here's some of the possible causes. So, IV therapy, acidosis, Cushing's syndrome, aldosterone. Okay, this is an issue I'm going to spend a second on. Why aldosterone? So, if you're releasing too much aldosterone, why is it cost hypernatremia?

Well, hypernatremia, remember, aldosterone is pulling in the sodium. Things like fever, sweating, respiratory infections, these are causing you to lose water, making your salt go up. Diabetes, diarrhea, kind of like I talked about before, you're losing water. And then a decrease in water intake can actually cause hypernatremia too. So, these are some possible causes. Manifestations, so water movement from intracellular to the extracellular fluid. So, it's shifting, kind of give-away that last slide, and then here are some of the symptoms I had on the last slide too.

And then hyponatremia, remember, can be too low salt or too high water as a cause. Overall, when they're measuring the sodium, they're looking at the sodium numbers, but there can be two possible causes. And then vomiting, diarrhea, GI. This is an interesting one too. I'm not going to spend a lot of time talking about the treatments or persnickety causes of some things. I'm trying to build your pathophysiology, not your clinical details. But when they give something like this, this is actually a sugar solution, this is dextrose So, when they give a sugar solution of dextrose, it will actually cause or could cause hyponatremia, drops your salt level or sodium level.

The reason is because if you remember from the GI tract in physiology, whoever you took physiology from, when you bring in a sugar particle, you bring in a salt particle. This is the blood brain barrier. When the brain brings in a sugar particle, it also brings in a salt particle or sodium particle. So, as you're pulling in the sugar into the brain, you're also pulling sodium out of the blood causing hyponatremia So they can actually use this as a treatment for hypernatremia, right? It's not actually fixing it. What's happening is by putting a sugar solution in their body, they're pulling some of the salt out of the blood and putting in other chambers like the brain. So, it's just something to think about when you look at the pathways or the physiology.

Right, next is chloride. So, what should I know about chloride? First, it's the primary extracellular fluid anion. It has a wet charge then, has a negative charge. Here are your regular values, 97 and 105 milliequivalents. It helps provide electroneutrality. So, when you're shifting around chloride, usually to help balance things out. If you remember the red blood cell, they actually called it the chloride shift. So, as chloride goes one direction, bicarbonate goes the other.

In other words, what charge was bicarbonate have if they're trying to move in opposite directions? They both have the same charge, keeping everything electrically neutral. So, here's bicarbon over here. As bicarbonate leaves red blood cell, chloride goes in, keeping everything electrically neutral. As bicarbonate comes back in, chloride leaves, keep everything electrically neutral. It's called the chloride shift.

And then when you look at chloride in general, it likes to follow sodium. You know this, because on your table, you have sodium chloride, which is table salt. They like to follow each other. They keep each other electrically neutral too, because the sodium has a positive, the chloride has a negative. So, when they stick together, they're actually neutralized. Chloride's really important because when it goes into nerves, it inhibits the nerves. When chloride flows in, it takes that resting potential, it makes it more negative. Remember, to depolarize, you make it more positive. So, it causes nerve inhibition, which is kind of important point.

When people take opiates, the opiates will actually allow chloride to go into a neuron, shutting them off, decreasing pain sensation. So, it's an important physiological point you want to keep in mind, right? And then even with acid-base balance, your stomach secretes hydrogen chloride. H+, Cl-, together, they're neutralized. When they get dumped in the water of the stomach, they separate. So, it helps regulate or neutralize acids. Sorry, I should, I should say hydrogen ion as we talked about acids in the next section.

So, a couple examples of chloride. One's a disease and one's something we use in practical reality. So, cystic fibrosis, the chloride transporter is broken. It's defective. So, as a genetic disorder, this transporter normally would move chloride back and forth, but something's wrong with it and it doesn't allow it to work. So, chloride will build up on the outside of their cells, and it won't go into the cells. When chloride builds up, it wants to hold sodium behind. When you have chloride and sodium hanging out here, what are they both going to attract? Lots of water. So, if you imagine this being the respiratory tract and they have all this sodium chloride sitting along the wall of their cells, it attracts water into the respiratory tract, causing a thick mucus to build up and it causes breathing problems.

You can think of the same thing with reproductive tract, the GI tract, the same thing. Chloride builds up on the outside parts of the body, which is the external environment, the lumen of whatever, lumen of respiratory, lumen of the GI tract, lumen of the reproductive tract. It causes this thick sticky mucus because chloride can't move. And then anesthetics, like I said something, one example is an opiate. So, opiates get in and what they do with that resting membrane is they bring it down here. So, opiates will allow chloride to come in and takes that resting potential and decreases it. So, what actually happens with opiates, so they decrease pain sensation, not completely shut it off.

And then chloride imbalances, hypo and hyper. General rule of thumb, with hypochloremia is usually common with hyponatremia. And then hyperchloremia is usually common with hypernatremia. So, they go hand in hand, and a lot of symptoms will come hand in hand too. Another problem here is acid-base balance. So, when you talk about that bicarbonate, remember HCO3 actually has a negative amount, you might want to draw that in. When you increase HCO3- in the blood, what should happen to chloride? Should it stay in the blood with all the other negative bicarbonate? No, it leaves. So, you kick it out.

So, hypochloremia, a lot of times you will see with an increased bicarbonate or an alkaline, which we'll talk about in the next section, the metabolic alkalosis. Because bicarbonate creates a very basic environment. So, hypochloremia, usually, you'll see signs of metabolic alkalosis at the same time, right? And then just the opposite, when you have a drop in bicarbonate, you have a rise in chloride. Oh, sorry, one more here. I don't know why… I just realized the numbers didn't come out right. But anyway, a third problem with hyperkalemia is when people take too many chloride diuretics. So, they're pumping lots and lots of chloride into the body and it causes issues.

So, next to the intracellular electrolytes. So, those are the primary extracellular. The first intracellular, remember, highest is going to be that potassium, huge. Remember why potassium is important? Every time that we've talked about action potentials or a change in electrical potentials, when we talk about depolarization, repolarization, potassium almost every time is revolving around repolarization. Sodium causes depolarization. Potassium across the board causes repolarization. It helps bring the cell back to stable. So, that's how you want to think about it.

Where's potassium primarily at? Inside the cell. So, what happens if you start increasing potassium outside the cell? Think about it. Potassium is high inside the cell. When you open doorways, potassium, it has a tendency to race out of the cell quickly. But what if it's crowded with potassium outside the cell at the same time? What's going to happen to speed of the potassium leaves? So, if potassium is high in a cell, potassium is high outside of a cell. So, here's a cell example. It's high here and high here. What's going to happen to the rate that it wants to leave? It doesn't leave very well. So, when you have too much potassium out here, outside the cell, it causes repolarization issues. The cell doesn't want to repolarize. So, keep that in mind.

I put both of these values in here. It's an intracellular fluid cation, positive charged. Inside the cell, it's about 156 milliequivalents, but when you take a plasma sample, you're actually looking at what's in the ECF. So, in a plasma sample, you should see about 3.5 to 4.5 milliequivalents for potassium. Definitely remember the physiological roles, I kind of covered that. I don't know what's going on with the slide here. So, maintains neutrality. It helps with that resting membrane potential. It also helps with repolarization. So, you want to think repolarization in cardiac, smooth. You want to think about neuromuscular skeletal and the neurons themselves.

Acid-base balance, the acid-base balances because potassium is a K+, there's actually a pump or a transporter that carries hydrogen and potassium. They both have the same charge. So, to keep electrically neutral, how do they have to move? Opposite to each other. So, we'll talk about this in a little bit more detail on a few slides in here. But as potassium is moving into the cell, hydrogen moves out.

So, when you think about this, if you're bringing potassium in, what kind of environment are you creating in the blood? An acidic environment, right? So, if an acidic environment is out here and your body starts putting the hydrogens into the cell, what's going to happen as result? Potassium gets kicked back out. So, watch the hydrogen and potassium. So, there's another ion exchange, hydrogen, potassium. What's the other ion exchange with potassium we talked about before, a special pump? Sodium potassium pump.

So, now you have to think about how the ECF potassium is regulated. There are a couple primary regulators. These you may not have heard of before. So, insulin, I know you've heard of insulin, but insulin affects potassium. When insulin comes out into the blood, it causes potassium to go into cells. So, insulin causes sugar to go into cells, but it also causes potassium to go into cells, right? So, when somebody has type 1 diabetes, they can't make insulin, what would you expect to happen with the potassium in their body? Will their blood stay high in potassium or will they go really low on potassium? Well, if they don't have enough insulin, you'd expect higher potassium levels in the blood.

When they take a big dose of insulin, what's going to happen to the potassium levels? They drop. Remember, potassium is important for life. It affects cardiac muscle, stability, so you could actually cause life threatening problems. Where do you get potassium? From your diet, you bring it in. How do you clear it primarily? Through the urine. So, diet again, GI tract and then urine. In between, you can put it in cells. You can maintain with things like insulin, catecholamines like norepinephrine. Don't forget norepinephrine and epinephrine. So, epinephrine, norepinephrine work a lot like insulin on potassium. They help you store it, they push it into the cells.

So, somebody is taking something like epinephrine, they take an EpiPen, what could you expect to happen to the potassium levels? Will they go up or go down? They go down, they drop. So, what happens to a potassium level after somebody takes a beta-2-agonist? So, a beta-2-agonist is increasing the activity of epinephrine basically, your epinephrine receptors. What would you expect to happen to the potassium levels? It goes down. But if they took a Beta-2 blocker, what would you expect? So, Beta-2 blocker, you expect to arise. And then here again, aldosterone.

So, affects the pH. I kind of talked about this on the last slide, but here you see that little pump again. Situations like acidosis, which we'll talk about in the next video. You want to kind of keep in mind, acidosis, hydrogen ions accumulate, acid accumulate. This is hydrogen as an acid. So, what would you expect to happen to potassium? As acid rises, the cells are going to pull hydrogen in. What are they going to do to potassium? Kick it back out, it'll kick the potassium out. So, in states of acidosis, you have to be careful, because potassium levels will start going up, causing heart issues. And then alkalosis, just the opposite. So, without those, you start pulling potassium into cell and kicking the acid back out. So, you'd see more hypokalemic situations. Wherein acidosis, you expect see hyperkalemic situations.

Some of the causes of hypokalemia, always think back about intake and output, reduced intake of potassium. You're not eating up bananas. That's not the only food with potassium, but you have to worry about an increased entry into the cells of potassium. So, potassium being kicked in, remember some of the causes, insulin, epinephrine, norepinephrine. And then loss of potassium. So, people taking lots of diuretics. Urinating a lot, they lose a lot of potassium. So, you have to worry about that.

Excuse me. So, manifestations of hypokalemia, what you're really going to look at is ECGs. Because remember, potassium has a huge impact on the heart. So, with neuromuscular and heart disorders, in this situation, neuromuscular with too little potassium, you get hyperpolarization, which means that there's weakness. It doesn't want to fire appropriately. The neurons are slowing down. When you look at the heart, what's interesting is that the heart has a special characteristic, this little thing called a U wave. So, it can cause dysrhythmias. The U wave is there because repolarization issues. It doesn't want to repolarize properly. So, you see a decrease in neural activity, weirdness in the heart, dysrhythmias. You see postural hypotension.

So, hypotension, because your neurons aren't firing properly. The sympathetic nervous system can't fire and also because the smooth muscles don't want to contract appropriately. So, when you stand up, instead of having those muscles and neurons responding and trying to squeeze blood vessels, they don't. Your blood pressure drops and potentially puts you in shock at some point too.

So, the treatment, I don't usually put treatments in, but as potassium intake but slowly like eating potassium or taking that calcium supplement. Because as you take it in slowly, your body can get rid of the excess. If you take it in quickly, you can actually cause your heart to stop. When we put people on the death chamber via lethal injection, we give them potassium chloride. We're giving them chloride to stop neurons, potassium to lose the repolarization phase. So, it stops their heart.

And then hyperkalemia, you can just kind of look at the opposite of hypokalemia. But some of the main causes, renal disease, because you can't get rid of the potassium. So, it builds up, it's kind of rare. Addison's disease, because Addison's disease affects aldosterone. So, Addison's disease, they don't have aldosterone. So, they're losing lots of sodium and retaining lots of potassium. I missed one, hyperkalemia, another one down here on the bottom. It's kind of important.

If potassium is primarily in the cells, what happens when you damage the cell? You see that potassium leak out, so it would be in the blood. So, like crush syndrome, when people crush large groups of muscles, those muscles released a potassium. After a heart attack, when the heart tissue dies, it releases potassium, you see hyperkalemic states.

And then the ECG on somebody with hyperkalemia. In this situation, you don't see that little U wave, but you do see a marked change in the T. So, if you remember here's your P. Q, R, S and T, that's normal. You don't usually see a U, but you see it with hypokalemia. In hyperkalemia, you actually see the polarization phase going up. It repolarize is a lot more dramatically. Remember, the T wave is ventricular repolarization. So, you have a huge spike in repolarization. And then here you can compare. Here's normal ECG. And then you can watch in hypo or decreasing potassium, you see that U wave starting to pop out. When you look at hyperkalemia, too much potassium, you can see the T wave gaining more pronounce and more peak. So, those are kind of trademark traits.

Don't give me that slide. Okay, calcium is the next one. Calcium, you really want to remember where calcium is at, primarily in the bone, a little bit in the blood and a little bit in the cell. So, 99% in the bone is hydroxyapatite stuff in the bone. When you look at the cells, you have 0.9% in the cells, and then that 0.1, a real teeny tiny percent. That 4.5 to 5.5 milliequivalents of calcium is in your blood, it's regulated. And then the main regulator is going to be parathyroid hormone. Yes, calcitonin helps regulate, but parathyroid hormone imbalances can cause death. So, you really want to pay attention to PTH. PTH cause your blood calcium to rise, go up.

So, if you are missing PTH, what happens to blood calcium? Yup, hypocalcemia. If you have too much PTH, what happens to your calcium? You get hypercalcemia, right? Calcitonin pulls calcium out of the blood and sticks it to the bone. So, PTH usually helps regulate the calcitonin. It's the PTH that can become life threatening, you really have to worry about it.

Before we go into the details of calcium disorders, I really want you to pay attention to the next one, phosphate. The key here is that when calcium rises, phosphate usually drops. They work inversely. So, when you see symptoms of hypercalcemia, you'll usually see symptoms of hypophosphatenia. When you see symptoms of hyporcalcemia, you usually see symptoms of hyperphosphatenia. They go hand in hand. So, it saves you a little bit of brain space. So, the phosphate levels are usually 2.5 to 4.5.

When you're looking at the phosphate again, where you bring in calcium and phosphate, you actually bring them both in from the GI tract at the same time. But when you lose them, you usually lose them disproportionately through the kidney. So, as you're kicking one out, usually you don't kick much of the other one out. Right. And then like I said before the inverse relationship, if you look at this as being constant So in the K+ isn't… Let's just focus on constant. If this is 10 as an example, if this level here is 2 and this is 5, it comes out to 10. But if you lower this down to 2, what do you have to do to this? You have to raise it to 5, they work inversely. So, as one goes up, the other one has to go down.

So, hypercalcemia, the first one. So, hypercalcemia, this is another truth about calcium. Calcium actually blocks sodium channels. So, when calcium and sodium in the right levels, everything works perfectly. But when you raise the calcium, it actually blocks sodium channels. So, what would you expect to happen to depolarization neurons? It goes down as a result. So, too much calcium causes neurons to decrease excitability. So, you see things like skeletal muscle weakness, cardiac arrest, so it turns them down. If you have too much calcium, your kidneys going to try and get rid of it, you're going to start seeing kidney stones. So, there are a couple main symptoms.

Causes, I already mentioned this, hyperparathyroid. Parathyroid dumps calcium into the blood, so it raises your calcium. Too much vitamin D, remember, vitamin D helps you absorb calcium. So, bringing lots of vitamin D will actually make you bring in more calcium. What's interesting in this is and what you want to pay attention to is that vitamin D also brings in phosphate. So, this is one of those rare situations where the same cause can cause issues with calcium being too high or phosphate being too high, right?

Another thing is where you store calcium in the bone. So, when you start breaking down the bone, it dumps the calcium in the blood. So, things like bone tumors or bone cancer can cause it. They're just the opposite. Hypercalcemia, so remember, without the calcium, there's less block to sodium. So, sodium moves into cells faster. So, you see increased neural muscular excitability. So, increased depolarization. You start seeing muscle tetany, muscle cramps, hyperactive muscle tissues. With breathing, you definitely don't want those breathing muscles going to tetany, because then you can't breathe.

Some of the causes of hypercalcemia is renal failure. So, you can't reabsorb calcium from the kidneys, not enough of the vitamin D, not enough of the PTH, maybe too much calcitonin coming out, not absorbing enough calcium. So, these are kind of common-sense things that you can just walk through and look at. So, I'm going to have you do is actually, there are two signs, two physical signs or interesting signs that happen with hypercalcemia. You're going to look at both the signs and explain to me why they both happen. So, both these happen with hypercalcemia and you're going to look them up. Go ahead and hit pause. You can use the internet, you can use your book, it's up to you.

Hyperphosphatemia, so I want you to think of first hyperphosphate is usually related or going to be associated with what about calcium? Low calcium, hypocalcemia. So, you can see a lot of same causes, you see a lot of seems symptoms. So, the best way to do this is go back and look at hypercalcemia. Some of the causes for hypophosphatemia is if the kidneys can't get rid of it, if cells are destroyed because there's lots of phosphate in the cells. So, when you see hyperphosphatemia, one of the first things you might want to look for being kidney issues or cell damage. And then if the cells destroy, what's the other intracellular fluid ion? Potassium. So, you might see high potassium and high phosphate indicating that there might be cell destruction, right?

And then hypophosphatemia, first, you want to look back at hypercalcemia. So, hypophosphatemia, not absorbing enough, vitamin D issues. Remember vitamin D helps you bring in phosphate, so not getting enough. And then things like antacid use can actually cause hyperphosphatemia, because the chemicals in the antacid bind the phosphate. They don't let you absorb it properly. Before I go into the next chemical, look at this. Antacids are high in magnesium.

So, what would you expect to happen to magnesium levels at the same time as low phosphate levels if it's because of an antacid? You probably expect the magnesium to go up while the phosphate goes down. That's if it's because they're taking too many acids. And then some of the symptoms. Remember calcium phosphate build bone. So, some of the symptoms would be weaker bones, muscle weakness. Phosphate is important for building the DNA inside of red blood cells. You might see bleeding issues, you might see anemia.

And then magnesium, the last one. Like I said, with magnesium, watch the acids, because usually magnesium issues are caused by antacid use. But magnesium, what it is there for is to actually helps calcium to work. So, on smooth muscles, it helps calcium move into smooth muscles. So, if you want to smooth muscle to contract, you let calcium in, which means you have to have calcium and you have to have magnesium present. It's also there for a lot of enzymes inside the cell to help regulate enzyme as a cofactor.

So, I skipped over one, sorry. It also binds to calcium or potassium receptors too. When you look at hypomagnesium, you want to go back and look at if you have too little magnesium, that means calcium is not going to work the same and potassium is not going to work the same. So, the symptoms are similar to hypercalcemia and hypokalemia. So, you get the neuromuscular irritability, the tetany convulsions etc. When you get hypermagnesium, what do you want to think of with calcium? It's going to be similar to what? Low calcium or high calcium? It will be similar to high calcium or high potassium. So, magnesium is pretty easy. Typically, the causes revolve around antacids.

So, taking away too many antacids in the situation. You can see the symptoms and the symptoms are going to be the same as the hypercalcemia too. So, here's the big picture, kind of keywords to help you remind what happens in low potassium or high potassium levels, key symptoms in low calcium, or high calcium. Then I had those two disorders you look up, and then phosphates and magnesium. So, they're all there for you. There are no more questions in this video set. I'll talk to you in the next video.