Chapter 16: Antimanic Drugs & Mood Stabilizers

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Welcome back to the Deep Dive.

Today we're doing something, well, a little different.

Yeah, a little more focused, I think.

Exactly.

Usually we take a really broad topic and kind of skirt around the edges, you know, picking out the fun facts.

But today - Right, we're getting our hands dirty.

We are rolling up our sleeves and getting technical.

We are cracking open chapter 16 of Psychiatric Nursing, seventh edition.

A classic text.

And honestly, a necessary one if you really want to understand the nuts and bolts of this profession.

It really is.

Specifically, we are looking at anti -manic drugs.

Now, I know what you're thinking.

You see that title and you think,

pharmacology, tables,

serum levels,

mechanism of action.

Boring.

The stuff that makes your eyes glaze over in a lecture.

Right.

But here's the thing.

And this is why we wanted to do the specific dive for you, the nursing student, or even just the lifelong learner who's interested in how we treat the brain.

This chapter is essentially the survival guide for managing bipolar disorder.

Absolutely.

And we really need to frame this correctly right from the start.

When you look at the whole landscape of psychiatric care, managing bipolar disorder is one of the most high stakes games a nurse plays.

High stakes is a good way to put it.

It is.

It's not just about, you know, pill counting or checking off a box on a chart.

It's about navigating a very, very narrow path between helping a patient regain their life and pushing them into toxicity.

It's like walking a tightrope, a very thin one with no safety net.

So our mission today is to unpack the tools used to treat the euphoric end of the bipolar spectrum.

We're talking about the heavy hitters, the big guns, lithium, the anti -convulsants and the anti -psychotics.

We are going to break down the mechanisms so they actually make sense.

No dry lectures here.

We're going to look at the safety protocols and we're going to really help you visualize what patient care actually looks like.

And we should probably clarify who we're talking to here.

You know, if you're prepping for your wards or maybe you're about to step onto a psych ward for your first clinical rotation, this is explicitly for you.

We want to take this dense, sometimes intimidating chapter and turn it into something you can actually use on the floor.

Because that's where it matters.

That's where it matters.

Because when you're standing in front of a patient who is manic, you know, pacing the hallway, maybe not making a lot of sense, you don't have time to flip through the index.

You need this knowledge locked in.

So let's start at the very beginning.

The text defines the disorder itself before it even gets into the drugs.

Bipolar.

Two poles.

Right.

Dysphoria and euphoria.

Depression and mania.

And the text makes a really interesting point right off the bat.

It says that while these seem like, you know, complete opposites, they're actually related.

They're two sides of the same coin.

It's not just that you have happy days and sad days.

It's a fundamental instability in the system.

It's a dysregulation.

Yeah.

They are deeply, deeply related.

And treating them requires this

comprehensive strategy.

It's not just take a pill and feel better.

The chapter outlines three overarching goals for Aitman that honestly every nurse needs to memorize because they guide literally everything you do.

Okay, let's walk through those.

What's goal number one?

First, you have to get the acute mania under control.

That's the immediate crisis.

The fire.

Exactly.

The patient is manic.

Perhaps they're dangerous to themselves or others.

They aren't sleeping.

They're impulsive.

Maybe spending money they don't have or engaging in really risky behaviors.

So you need stabilization.

Fast.

You need to put the fire out.

That's job one.

Right.

That's the emergency response phase of care.

Exactly.

Then once the fire is out, you move to goal number two, which is preventing relapse when remission occurs.

Because it's a cyclical disorder.

It will come back if you don't have a wall built up against it.

So this is where your maintenance therapy comes in.

This is the long game.

And third, and I think this is the one we sometimes forget in the chaos of the hospital environment,

is returning the patient to their prior level of functioning.

This is so crucial.

We want them back to their social lives, their jobs, their relationships.

It's not just about sedation.

It's about restoration.

That's a great distinction.

Think about it.

If you stop the mania, but the patient is so sedated, they can't work or they can't interact with their family.

Or if they have tremors so bad, they can't hold a coffee cup.

Have you really succeeded?

Exactly.

Have you actually helped?

That's the question you have to ask.

That's a great point.

We aren't trying to turn them into zombies.

We are trying to give them their lives back.

Precisely.

That's the entire goal.

Okay.

So with those goals in mind, let's get into the protagonist of our story today.

The text literally calls it the gold standard.

It's a drug that has a backstory that sounds like it was written for a movie.

We are of course talking about lithium.

Lithium.

It really does have this unique, almost mythic position in psychopharmacology.

The text notes that it actually preceded the modern era of psych drugs.

Before everything else.

Before we had chlorpromazine, before the big anti -psychotics or the SSRIs that everyone knows today, we had lithium.

And what I love, what I think is so cool about this, is the name origin,

lithos.

Greek.

It's Greek for stone.

That's what it is.

It's an element.

It's on the periodic table right there with sodium and potassium.

It's not some synthesized compound cooked up in a lab in the 1990s with a crazy chemical formula you can't pronounce.

It's a salt.

It was discovered way back in 1817.

And initially they used it for all sorts of random things.

They were throwing it at everything.

Epilepsy, bladder stones.

It was the early 19th century.

So medical science was a lot of, let's see what happened.

A lot of trial and error.

A lot of error.

They thought maybe it dissolved stones in the body because of the name or helped with uric acid.

But the real turning point, the moment that changed psychiatry forever happened in 1949.

And this is where John Cade enters the story.

Yes, John Cade.

An Australian researcher.

He was working in a repatriation hospital after World War II with veterans.

And he was looking for the cause of mania.

He had this theory that mania was caused by a buildup of some toxic substance in the body, specifically in the urine.

So his idea was that your body was poisoning itself into a manic state.

That was the hypothesis.

So he started injecting guinea pigs with urine from manic patients to see if it would make them manic.

Which is a choice.

I mean, science is messy, but that's a specific kind of messy.

It is a very specific kind.

But here's the serendipity.

Here's the lucky break.

To make the uric acid in the urine soluble so he could inject it, he used lithium urate.

So he wasn't even testing the lithium?

No.

He was just using it as a delivery vehicle, a means to an end.

But he noticed something really strange.

What was that?

The guinea pigs didn't get agitated.

They didn't get manic.

They got lethargic.

They got calm.

They just kind of laid there.

They chilled out completely.

Exactly.

They became profoundly calm.

So Cade, being the bold researcher he was, thinks, huh, maybe it's the lithium.

He eventually moved to human subjects.

That's a big leap.

A huge leap.

And in 1949, he reported in the Medical Journal of Australia that lithium was effective for manic depression.

He actually got such dramatic, unbelievable results that he called the illness a lithium deficiency disease.

Which is a bold claim.

It's like saying you have a scurvy style deficiency of a rock.

A very bold claim.

And scientifically, we know now that's not quite accurate.

You don't have a deficiency of lithium in a biological sense like you do with vitamin C or iron.

Right.

But it showed how powerful the effect was.

All of his manic patients showed improvement.

For people who had been locked away in asylums maybe for years, this was a miracle.

An absolute game changer.

But here's the plot twist.

And the text highlights this specifically.

John Cade publishes this in 1949.

A monumental discovery.

But lithium isn't approved in the United States until 1970.

That is a 21 -year gap.

That is a lifetime in medicine.

Think of how many people could have been helped in those two decades.

So why?

Why the delay?

If it worked so well in Australia and in Europe, why were we just sitting on our hands in the U .S.?

Well, the expert breakdown here is really twofold.

And it's a mix of tragedy and economics.

Okay.

First, the tragedy.

In that same year, 1949,

the Journal of the American Medical Association, JAMA, published these reports of fatal poisonings.

Oh, wow.

From the psychiatric patients.

Cade's patients.

No.

And that's the real tragedy of it.

It wasn't psychiatric patients at all.

It was cardiac patients.

Cardiac patients?

What were they doing with lithium?

People were using lithium chloride as a salt substitute.

A salt substitute.

You mean like, I can't have sodium because of my heart, so I'll put this on my eggs instead.

Exactly that.

Yeah.

If you had heart disease or hypertension,

your doctor told you to avoid sodium.

So companies started selling lithium salts as a replacement to make food taste salty.

And does it?

It tastes just like salt.

So people were just sprinkling this stuff on their dinner in completely uncontrolled amounts.

And as we're about to learn in detail, lithium has an incredibly narrow therapeutic window.

They were overdosing massively.

And they died.

Many did.

It was extremely toxic in those quantities.

So immediately the U .S.

medical community just said, whoa, this stuff is dangerous.

It kills heart patients.

So the FDA banned it.

Fear was factor number one.

Okay.

That makes sense.

Very tragic sense.

And factor number two?

Money.

Of course.

The text is very cynical, but, you know, accurate about this.

Lithium is a natural element.

It's a mineral you dig out of the ground.

You cannot patent a rock.

So the drug companies looked at it and said, we can't own this.

Can't own it.

So we can't make an exclusive profit from it.

Why would a company spend millions and millions of dollars running the massive clinical trials required for FDA approval?

If any other chemical company can just mine it and sell it the next day?

Exactly.

There was zero financial incentive to prove it was safe for bipolar disorder.

That is incredibly frustrating.

It just really shows you how economics impacts patient care on a fundamental level.

It absolutely does.

So, you know, between the genuine fear of toxicity and the complete lack of a profit motive, it just sat on the shelf in the U .S.

for two decades while Europe and Australia were using it to change lives.

So what changed?

How did it finally get approved?

It took tireless advocacy from researchers who saw the results coming out of other countries and just refused to let it go.

They fought for years to finally get it approved here in 1970.

That is a wild history, but eventually it gets here.

And today, despite all the fancy new drugs we're going to talk about later, the text says it is still the king.

It is.

The text says it's effective for about 50 % of acute cases and up to 80 % for long -term prophylaxis, which just means prevention.

So for keeping people well.

Right.

If you can tolerate it, and that's a big if, it works incredibly well.

And there's one other unique benefit the author mentions that is absolutely crucial for nurses to know.

What's that?

Lithium has a specific anti -suicide effect.

Really?

More so than other drugs.

Yes.

Multiple studies have shown that lithium reduces suicidality, both the thoughts, the ideation, and the actual attempts, more effectively than other anti -manic drugs.

Wow.

For a disorder with such a high suicide risk like bipolar, that is a massive, massive nugget of information.

It essentially protects the patient from their darkest impulses in a way other drugs don't seem to.

That's huge.

Okay, so we know it works.

We know its history.

But the million dollar question, and the part that usually trips up students on exams, is how it works.

The mechanism of action.

The big MOA.

The text admits that exactly how it works is technically unknown, which is usually science speak for.

We have some really strong theories, but not a perfect map.

But it offers some very good models.

I like to think of lithium as the imposter.

That's a really good analogy.

I like that.

It's an imposter for other minerals in the body.

It looks like potassium, it looks like calcium, but mostly it looks like sodium.

Right.

It shares that same first column on the periodic table.

And because it looks so much like these other essential ions, it can kind of sneak into the cellular processes where it doesn't belong.

And mess things up in a good way.

Exactly.

Let's look at the biogenic amine theory first, which connects to figure 16 to 1 in the text.

Okay, walk us through that.

So the basic theory of mania for a long time was that it's essentially an overabundance of amines neurotransmitters, like norepinephrine, serotonin, and dopamine acting at the receptors.

So too much signal.

Way too much signal.

Think of it as a loud party in the brain.

Everyone is shouting, the music is blasting.

The volume is turned up to 11.

Exactly.

Lithium acts like a bouncer at this party.

First, it inhibits the release of these neurotransmitters.

Okay.

It stands at the door of the neuron and says, hey, stop throwing so much dopamine out there.

Okay, so it slows down the release.

But it does something else too.

It facilitates their reuptake.

Explain reuptake for us.

What does that mean in this party analogy?

Imagine someone spilling a drink at the party.

Reuptake is the cleanup crew coming in with a mop and a vacuum and getting it off the floor quickly.

Lithium helps the presynaptic neuron, the one that released the chemical vacuum, it back up faster, clearing out the synapse.

So less chemical being released in the first place and a faster cleanup of what does get released.

You got it.

Both actions work to quiet the noise.

That makes sense.

But that's just the surface level.

If you want to really impress your professor or really understand the drug on a deeper level, you need to look at the second messenger system.

Okay, let's unpack this.

This is where eyes usually glaze over in lecture.

Make it real for us.

Okay, think of the neurotransmitter, the dopamine, for example, hitting the outside of the cell wall as the doorbell ringing.

That's the first message.

Ding dong, someone is here.

Okay.

I'm the cell.

I hear the doorbell.

Got it.

The second messenger is the system inside the house that hears the doorbell and then goes and does something about it, like turning on the lights or opening the door or telling the dog to bark.

It's the internal response system.

In bipolar disorder,

this intracellular system is hyperactive.

The doorbell rings once and the whole house goes crazy.

The lights start flashing like a disco.

The music starts blasting.

The dog is barking.

The sprinklers on the lawn go off.

Exactly.

The internal reaction is completely disproportionate to the external signal.

Lithium comes in and resets this internal system.

Specifically, the text mentions it prevents the full expression of inositol.

Inositol?

What's that?

Inositol is a lipid that's a key part of that second messenger system.

Its job is to signal for calcium to be released inside the cell.

And calcium is what acts as the trigger for the expulsion of more neurotransmitters.

Okay, so let me see if I can trace the chain here.

Lithium lowers inositol.

Lower inositol means less calcium is released inside the cell.

Correct.

And less calcium means the cell stops spitting out so many neurotransmitters.

You've got it.

It calms the internal reaction of the neuron.

So now when the doorbell rings, the house just answers the door quietly.

That makes so much more sense.

It dampens the amplification inside the cell.

That's a perfect way to describe it.

There is one more model in the text that I found absolutely fascinating.

The ion dysregulation model by L.

Mollock.

This tries to answer the question, what actually goes wrong in bipolar?

This is a really compelling model because it tries to explain the whole cycle.

Not just the mania.

Right.

It suggests that the root cause is a disruption in the sodium potassium ATPase pump.

The Na plus K plus pump, the battery of the cell.

I remember this from Bio 101.

Exactly.

It's fundamental.

Its job is to keep sodium out and potassium in.

It maintains the electrical charge in the neuron, its readiness to fire.

So what does this model say goes wrong?

In mania, this model suggests the pump's activity decreases.

It gets lazy.

When the pump gets lazy, sodium starts to accumulate inside the cell.

This changes the resting potential of the neuron.

It becomes irritable.

It becomes hyper excitable.

It fires way too easily.

So a lazy pump leads to a twitchy, irritable neuron.

Yes.

A tiny little signal can set it off.

And lithium's fix in this model is that it substitutes for sodium and it actually boosts the pump's activity.

It helps normalize that ion exchange, creating a higher threshold for firing.

It makes the neuron harder to trigger.

And does this model explain the crash, the depression that follows?

It does.

And this is the really elegant part.

The model suggests that as the pump continues to fail further, the neuron fires easily, but the strength of the signal, the action potential, gets weaker and weaker.

It's firing a lot, but the bullets are getting smaller.

Perfect analogy.

Eventually, the calcium channels stop working properly, neurotransmitter release drops way down, and you crash into depression.

In the most extreme cases, the system just stalls out completely, which might even explain catatonia.

That is a really elegant way to connect the highs and the lows.

It's not two different problems.

It's the same broken pump, just at different stages of failure.

Exactly.

And lithium is a mechanic that comes in and helps fix the pump.

It stabilizes the very foundation of the neuron's ability to fire correctly.

Okay, let's move from the brain to the body.

Because if you are a nurse administering lithium, you need to be obsessed with one particular organ, and it's not the brain.

It's the kidneys.

Let's get into the pharmacokinetics section.

Okay, so lithium is absorbed well in the GI tract.

Keek levels happen in about one to three hours.

But here's the critical nursing point, maybe the most important single sentence we've said so far.

Lithium is not metabolized.

Say that again for the people in the back.

Lithium is not metabolized.

Your liver doesn't touch it.

It enters your body as a simple element.

And it leaves your body as a simple element almost exclusively.

We're talking more than 95 % through the kidneys.

Which means if your kidneys aren't working, you are in big, big trouble.

Renal disease extends the half -life of the drug significantly.

A typical half -life is about 24 hours.

But if your kidneys are compromised, or even if you're just elderly, and your filtration rate is naturally lower, that drug stays in your system.

Building up and up and up to toxic levels.

And this brings us to the famous seesaw.

The relationship between sodium and lithium.

This is probably the most practical day -to -day thing a patient on lithium needs to understand.

It is the golden rule of lithium safety.

The kidneys handle lithium and sodium in very similar ways.

To the renal tubules, they look almost identical.

They can't tell them apart.

They compete for the same exit door, essentially.

So explain the seesaw.

What happens on each side?

Okay, so if your sodium intake is low, let's say you go on a crash diet.

Or you decide to avoid all salt because you think it's healthy.

Or you get a stomach flu and have a lot of vomiting and diarrhea.

You're losing sodium.

Right.

Your kidneys panic.

Their programming says, we're losing salt.

We need to conserve salt to survive.

So they start hoarding it.

And because they can't tell the difference, they hoard lithium right along with it.

So low sodium equals high lithium retention in the body.

Which leads directly to toxicity.

Correct.

And the reverse is also true.

If you eat a huge salty meal, a big pizza, bag of potato chips, Chinese takeout.

Or sodium level spikes.

Your kidneys say, whoa, too much salt, get rid of it.

So they open the floodgates and start dumping sodium in the urine.

And they dump lithium right along with it.

So high sodium equals low lithium levels in the blood.

Which means your levels become subtherapeutic, the drug stops working, and the mania can come roaring back.

Exactly.

You have to keep the seesaw balanced.

You cannot have wild fluctuations in your salt intake.

Consistency is everything.

The text has a critical thinking question that illustrates this perfectly.

It's about a guy named Johnny.

Right.

The 23 -year -old basketball player.

So let's look at this scenario.

Johnny is on lithium.

He plays ball four times a week and he sweats profusely.

The text asks, what is the nurse concerned about here?

Well, let's just walk through the physiology.

When Johnny is sweating on the basketball court,

what is he losing in that sweat?

Salt and water.

A lot of salt and water.

He is losing sodium through his sweat.

So if his sodium levels in his blood start to drop, what are his kidneys going to do?

They are going to try to compensate by retaining what they have left.

And in doing so, they're going to retain the lithium too.

Exactly.

So Johnny could go to practice, sweat buckets, and if he only rehydrates with plain water, which dilutes his system even further, he could come home, take his normal dose of lithium that evening, and wake up toxic.

Wow.

Absolutely could.

The nurse's job is to teach him that he needs to replace both fluids and electrolytes.

Just drinking water isn't enough because that dilutes the sodium even more.

He needs a sports drink with electrolytes, or he needs to make sure his dietary salt intake is adequate to match his loss from sweating.

It's such a delicate, delicate balance.

It's not just take two pills and call me in the morning.

It's take two pills, drink 10 glasses of water.

Don't change your diet and be really careful how much you sweat.

It is a lifestyle commitment.

You can't just take the drug and forget about it.

It requires constant vigilance from both the patient and the nurse.

Let's talk numbers.

Nursing students love numbers because they are concrete.

They're easy to memorize for the test.

But these numbers are life and death.

What is the therapeutic window for lithium?

It is notoriously, famously narrow.

You need to burn this into your brain.

0 .6 to 1 .2 Meql.

0 .6 to 1 .2.

Got it.

Ideally, for maintenance, we like to see it around 0 .8.

For an acute manic episode, we might push it a little higher, maybe up to 1 .5 to get control.

But that is very risky.

You are dancing on the absolute edge of the cliff at that point.

And where does the danger zone officially start?

Toxicity effectively begins at anything over 1 .5.

And once you cross 2 .0, you are in moderate to severe toxicity.

And it doesn't take much to slip from a therapeutic 1 .2 to a toxic 2 .0.

No.

That's a missed meal, a stomach flu with some vomiting, a really hot day outside.

That is a razor -thin margin of safety.

Now, even in that safe zone of 0 .6 to 1 .2, patients aren't feeling perfect, right?

What are the common side effects that we just have to manage?

Right.

Even at therapeutic levels, you're going to see a lot of side effects.

Nausea, dry mouth, some diarrhea, thirst, and a mild hand tremor.

That fine little tremor is very, very common.

It's annoying, but it's not dangerous.

And the thirst.

The text mentioned that's a big one.

Polyuria and polydipsia, excessive urination and excessive thirst.

The text says this occurs in 70 % of patients.

70 %?

That's almost everyone.

It is.

I mean, imagine drinking water constantly and having to pee constantly all day every day.

It's incredibly disruptive to your life.

And then on top of that, there's the weight gain, the edema, and the cognitive dulling or mental fogginess.

Let's talk about that for a second.

The cognitive dulling.

Patients often complain they feel less sharp, less creative, like their mind is moving through mud.

Which has to be a huge compliance issue.

If you're an artist or a writer or just anyone who relies on their creativity and you feel like the drug is stealing your spark, you're going to stop taking it.

Exactly.

They start to miss the mania because the mania made them feel brilliant and alive and creative.

And the lithium makes them feel flat or dull.

Now, there are some other adverse reactions that aren't just about the dose, but about how the drug affects other systems in the body.

We mentioned the thyroid.

Yes, lithium can cause hypothyroidism.

It basically gives you a goiter.

How common is that?

It occurs in about 30 % of patients.

The lithium interferes with thyroid hormone production and release.

So you might need to add levothyroxine, a thyroid hormone, to their regimen.

So now you're taking a pill to fix the side effect of the other pill.

It's a classic pharmacology cascade.

Yeah.

And then there's this other condition with a very long name.

Nephrigenic diabetes insipidus, NDI.

And this is different from sugar diabetes.

Completely different.

It has nothing to do with blood sugar.

This goes right back to the kidneys.

Lithium can block the action of ADH antidiuretic hormone.

And ADH is the hormone that tells your kidneys to hold onto water so you don't dehydrate.

Right.

It's the anti -P hormone.

So if lithium blocks the hold water command, the floodgates open.

The patient just dumps massive amounts of dilute urine.

We're talking more than three liters a day.

It's relentless.

And obviously, if you're paying that much, you are going to be incredibly thirsty, hence the polydipsia.

Exactly.

If this happens, often the lithium has to be stopped, or at least reduced, because it's so disruptive and can be dangerous for their fluid and electrolyte balance.

The text also references a paper by Keltner and Grant about neuropathy.

Yes, irreversible neuropathy.

It's rare, but there are documented cases where long -term lithium use has caused permanent nerve damage.

It's a sober reminder that this is a heavy metal we are putting into the body.

It's not benign.

It accumulates over time.

OK, let's move to the scary part.

Toxicity.

As a nurse, you are the early warning system.

You have to be the one who spots the difference between, I am having a side effect and I am actively being poisoned.

And the signs can be subtle at first.

The text breaks us down into tiers based on the serum levels.

We mentioned that 1 .5 to 2 .0 MEQL is considered mild to moderate toxicity.

What does that look like in a patient?

The key sign here, the one you have to watch for like a hawk, is the change in the tremor.

A therapeutic tremor is fine.

A toxic tremor is coarse.

Can you describe the difference for the listeners?

How would you know?

OK, a fine tremor is like holding a sheet of paper out and seeing it vibrate just slightly.

You might have trouble threading a needle or your handwriting might get a little shapey.

A coarse tremor is a visible, shaky, jerky movement of the hands.

They'd have trouble holding a cup of water without spilling it everywhere.

So it's much more pronounced?

Much more.

Along with that coarse tremor, you'll see severe diarrhea, vomiting, confusion, and a lack of coordination, what we call itaxia.

They might look like they're drunk.

OK, so if the patient is stumbling, spilling their water, and running to the bathroom, we are in deep trouble.

What about the next level,

moderate to severe?

That's when the level is between 2 .0 and 3 .0 MEQL.

Now the symptoms escalate significantly.

Giddiness, which can be confusing because they're bipolar, so you might mistake it for emerging mania.

But also tinnitus, a ringing in the ears, blurred vision, and a large output of very dilute urine.

Delirium sets in.

They aren't just confused.

They're really out of it.

And above 3 .0.

Severe toxicity.

This is a life -threatening medical emergency.

You're looking at seizures, organ failure, coma,

death, the kidneys shut down, the heart rhythm scrambles.

It's a systemic poisoning.

There is a case study in the text that really drove this home for me.

The story of Bill.

This is a heartbreaking story, but a necessary one for every nursing student to read.

It illustrates just how easily and tragically this can go wrong.

So what happened with Bill?

Bill was a 38 -year -old man.

He was incarcerated, and he had bipolar disorder.

And the whole problem started with compliance, right?

Exactly.

Before he was in jail, he was telling his prescriber that he was taking his meds every day.

But he wasn't.

So every time they checked his blood, his levels were constantly low, subtherapeutic.

So the doctor, thinking Bill is taking the pills, but just metabolizing them weirdly or not absorbing them well, just keeps upping the dose.

Precisely.

The doctor is treating the lab number, not the patient.

They keep increasing the prescription to try to get that blood level into the therapeutic range.

They eventually got him up to 2 ,100 milligrams a day.

That's a huge dose.

A massive dose.

Usually we're talking about 900 to 1 ,200 milligrams for maintenance.

2 ,100 is huge.

But Bill wasn't actually taking it.

Until he went to jail.

Right.

In jail, you don't have a choice.

The officers watch you take your meds to ensure compliance.

So suddenly, Bill goes from taking 0 milligrams a day to actually taking 2 ,100 milligrams of lithium a day.

And his body just couldn't handle it.

He became toxic very, very quickly.

But because he was in a jail setting, maybe the signs weren't caught instantly or were misinterpreted.

He went into a coma for six weeks.

Six weeks.

That is terrifying.

The text notes, he permanently lost the ability to walk.

He had permanent neurological damage.

He went from being a 38 -year -old man with a treatable illness to being permanently disabled because of a dosing error based on misinformation.

The lesson there is just so profound.

Treat the patient, not just the lab number.

And you have to listen to the patient's history.

And you have to verify compliance.

If a dose seems astronomically high, but the blood level is still low, your first thought shouldn't be weird metabolism.

It should be noncompliance.

You have to ask the hard questions before you just keep writing larger and larger numbers on the script.

So let's say a patient like Bill presents in the ER.

They're toxic.

How do we fix it?

Is there an antidote we can give them?

There is no specific antidote.

There's no lithium -begone shot you can give.

It's all about supportive care.

So what do we do?

What are the interventions?

If it's very early and they just took the pills, you could do a gastric lavage pumping the stomach.

But usually by the time they're symptomatic, it's too late for that.

So mostly we need to correct the ions and help the body get rid of it.

We give them IV saline to provide sodium and volume.

Remember the seesaw?

Giving them sodium helps the kidneys excrete the lithium.

For severe cases, we use forced diuresis or even hemodialysis.

So you have to actually filter their blood.

We essentially have to wash the blood to get the metal out.

It's an aggressive treatment for an aggressive life -threatening toxicity.

That brings us to the how -to for the nurse on the floor.

Box 16 -2 in the text is basically a checklist for patient teaching.

If you are discharging a patient on lithium, what are the absolute must -help points?

Let's go through the checklist.

Okay.

First and foremost,

consistency.

Take it at the same time every day.

And if you miss a dose, do not double up on the next one.

Why not?

Doubling up is a one -way ticket to spiking your level and getting toxic.

Just wait for the next scheduled dose.

Okay.

What second?

Second.

The salt and water talk, again and again.

Drink 10 to 12 glasses of water daily and maintain a consistent salt intake.

Do not decide to go on a low sodium health kick without talking to your doctor.

That's so counterintuitive for a lot of people who are always told that salt is bad for you.

It is, and you have to explain why it's different for them.

Third,

take it with food to help with the nausea.

And fourth, and this is maybe the most important, know the red flags.

The signs of toxicity.

Yes.

If you are vomiting, if you have a severe tremor, not the fine one, the coarse one, or if you feel really sedated or have muscle weakness,

you call the doctor immediately.

Do not wait.

What about pregnancy?

What do we tell patients about that?

It's FDA category D.

That means there is positive evidence of human fetal risk.

Specifically, it's linked to cardiovascular malformations in the first trimester, a rare one called Epstein's Anomaly.

But the text notes there's a real dilemma here for clinicians.

Right.

The risk of those abnormalities is about 4 to 12 percent on lithium.

The general population risk is 2 to 4 percent.

So it's higher, but it's not 100 percent.

The dilemma is that uncontrolled mania during pregnancy is also really dangerous for the fetus.

A manic mother might not eat.

She might be physically reckless.

So sometimes the risk of the drug has to be weighed against the risk of the illness itself.

It's a risk benefit analysis.

Always.

And for breastfeeding.

What's the guidance?

Lithium is present in breast milk at significant levels.

It's generally discouraged because a newborn baby's kidneys are immature and they can't handle that load.

Okay.

That is lithium.

The gold standard.

But as we said, it doesn't work for everyone.

Or the side effects are too much to tolerate.

Or the patient has kidney disease and can't take it.

So we have to turn to the second class of drugs.

The anticonvulsants.

Which, you know, begs the obvious question.

Why are we giving epilepsy drugs to people with mood disorders?

I love the analogy the text uses to explain this.

Kindling.

Yes.

The kindling theory.

It's a great model.

Think of building a campfire.

You don't start by lighting a giant log.

Right.

You start with small twigs kindling.

A little spark catches a twig.

If you don't put it out, that little flame spreads to the branches, then to the logs, and soon enough you have a raging, out -of -control fire.

And the brain is the campfire.

The brain is the campfire.

In epilepsy, small abnormal electrical activities.

The sparks spread to create a seizure.

In bipolar, this theory suggests that stress or small chemical changes act as sparks.

If they catch, they spread and ignite a full manic episode.

So anticonvulsants are essentially like a fire retardant.

That's a perfect way to put it.

They raise the threshold.

They make the wood damp, so to speak.

They make it much harder for the spark to catch and spread.

They stabilize the electrical activity of the brain so the mood doesn't swing so wildly.

And what are the mechanisms they use to do that?

They're a bit different from lithium.

A big one is that they increase GABA.

GABA is the brain's primary inhibitory neurotransmitter.

It's the chill -out chemical.

It's the brakes.

So they put the brakes on the brain.

Right.

They also block voltage -gated sodium and calcium channels, which just generally dampens the excitability of the neurons.

Okay, let's run through the roster of these drugs.

First up, Valprotes, Divalprox, or as most people know it, Deepakote.

This is a really common one.

In fact, it's often the first choice agent now, even before lithium for many clinicians.

Why is that?

What are the advantages?

It works faster than lithium.

It has a more rapid onset.

It's generally well tolerated.

And it doesn't have as much of that cognitive dulling that people really hate with lithium.

But it's not without its own baggage.

What are the side effects?

No, it's not.

Common side effects.

Hair loss alopecia, which is usually transient.

It often grows back, but it's very distressing for patients.

I can imagine.

And weight gain, GI upset.

But the really serious risks are the ones you need to watch for on the lab work.

The first one listed is thrombocytopenia.

Which is low platelets.

Your blood can't clot properly, so you need to watch for easy bruising or bleeding.

If a patient tells you they're brushing their teeth and their gums are bleeding a lot, you need to check their platelet count.

And the liver.

It can be tough on the liver.

Very tough.

Hepatotoxicity and pancreatitis.

You need to be monitoring their liver enzymes, their AST and ALT, and their amylase.

There was a specific and really important update in the text regarding pregnancy and valprotes in a box called Highlighting the Evidence.

Yes, this is critical for nurses to know.

The FDA changed the pregnancy category from D to X for one specific use.

Migraine prevention in pregnant women.

And category X means?

It means the risk absolutely outweighs any possible benefit.

Do not use.

Why the change?

There was new data that showed that children who were exposed to valprode and utero had significantly lower IQ scores later in life.

Now for bipolar and epilepsy, it remains category D because the risk of stopping the drug might be worse.

Seizures or full -blown mania are also very dangerous for a fetus.

But for something like migraines, the risk isn't worth it.

Okay, next drug on the list.

Carbamazepine or Tegretol?

This one is often the go -to for rapid cyclers.

And what does that mean?

Patients who cycle up and down very quickly, maybe having four or more episodes a year, they often don't respond well to lithium, but for some reason they respond really well to Tegretol.

What's the major warning here?

The big red flag.

A granulocytosis.

Say that again?

A granulocytosis.

It's a dramatic and dangerous drop in white blood cells.

Which means the patient loses their ability to fight infection?

Exactly.

A common cold could become pneumonia.

So the nursing action is mandatory weekly CBC complete blood count monitoring, especially when they first start the drug.

If they call you with a sore throat or a fever, you don't just say take a lozenge,

you tell them to come in immediately to get their blood checked because it could be life -threatening.

Okay.

Next, Lamotrigine or Lamictal?

I feel like I see this one prescribed a lot these days.

It's very popular, especially because it seems to be better for the depressive side of bipolar than some of the other mood stabilizers.

It works by inhibiting glutamate, which is an excitatory neurotransmitter, but it have one massive flashing neon red light of a side effect.

The rash.

The rash.

Stevens -Johnson syndrome.

And we need to be clear.

This isn't just a little patch of itchy skin.

This is a life -threatening systemic skin condition where the skin and mucous membranes essentially blister and peel off.

It's a burn unit sandwich.

That's terrifying.

It is.

So if a patient on Lamictal calls and says, hey, I have this new rash on my chest.

You stop the drug immediately and tell them to get evaluated.

Immediately.

Do not pass.

Do not collect $200.

Get to an ER.

The risk factors for this are starting at too high a dose or escalating the dose too quickly.

You have to titrate Lamictal very, very slowly to let the body adjust.

We're talking weeks to get to a therapeutic dose.

And finally, in this anticonvulsant group to Pyramate or Topamax.

This one is really interesting because unlike every other drug we've discussed so far, a major side effect is weight loss.

Which must sound great to patients who are gaining 20 pounds on lithium or Depakote.

It does.

It sounds like a miracle.

But the trade -off is often significant cognitive side effects.

The text implies the nickname Dopamax.

It can make people feel a bit dopey.

Dopamax.

Cognitive dulling, word finding difficulties.

Patients will say they know what they want to say, but they just can't find the word.

Dopamax.

I'll definitely remember that.

OK.

That brings us to the third category of drugs used.

The antipsychotics.

Now we did a whole deep dive on these in Chapter 14, but why are they showing up here in the bipolar chapter?

For two main reasons.

The first one is speed.

As we said, lithium takes 7 to 10 days to really reach therapeutic levels.

Valproats take a few days.

If a patient is carrying up the ER right now in a state of acute mania, they're jumping on tables.

They haven't slept in four days.

You don't have 10 days to wait.

You need an anchor.

And you need it now.

You need an anchor now.

Antipsychotics work fast to sedate and control the agitation and psychotic symptoms of mania.

So they're often used as a bridge.

You start the lithium and the antipsychotic at the same time.

Once the lithium kicks in and stabilizes them, you might be able to taper the antipsychotic off.

And the second reason they're used.

They actually work as maintenance mood stabilizers in their own right.

Several of them, like olandipinezaprexa and arpiprazoleabilify, are FDA approved for the long -term maintenance treatment of bipolar disorder.

They help keep the mania away.

But again, they come with their own set of significant side effects, olandipine.

Weight gain.

Significant, often dramatic weight gain.

And with that comes metabolic syndrome.

You have to be watching their blood sugar, their lipids, their waistline.

It can cause diabetes and eye cholesterol.

And arpiprazoleabilify.

It's what they call a third generation or new second generation antipsychotic.

It's generally better tolerated with less weight gain, but it can cause akathisia.

That's that inner restlessness.

Yes, that horrible feeling where you feel like you want to crawl out of your skin.

You just can't sit still.

And clozapine is also mentioned.

Clozapine is the nuclear option.

It's incredibly effective for treatment -resistant cases that haven't responded to anything else.

But it carries that risk of agrandulocytosis, just like carbamazepine.

It requires enrollment in a national registry for constant blood monitoring.

So putting this all together, the treatment for bipolar disorder isn't usually just one pill.

No.

Monotherapy using just one drug is the ideal.

But in reality, combination therapy is very, very common.

You might see a patient on lithium plus an antipsychotic or Deepakote plus an antipsychotic.

The text mentions table 16 -2, which breaks down the evidence for these drugs.

And it's interesting because not all drugs work for all phases of the illness.

Right.

And this is where the real art and science of psychopharmacology comes in.

For example, Lamotrigine is weak on controlling acute mania.

You wouldn't use it to stop a full -blown manic episode.

But it's very strong on maintenance and protecting against future depression.

And lithium.

Lithium is strong on mania and strong on maintenance, but maybe a little less effective on its own for an acute severe bipolar depression without some help from another agent.

You have to match the drug to the specific phase of the illness the patient is in.

So as we start to wrap up this deep dive, I want to recap the essential study notes for the students listening.

Let's boil this entire chapter down to the absolute essentials you need to carry with you onto the floor.

Let's hit the high points, the must -knows.

Point one, mechanisms.

Lithium acts on intracellular conductance.

When you think lithium, think ions, think the second messenger doorbell inside the cell.

And anticonvulsants act on GABA and ion channels.

When you think of them, think calm, think fire retardant.

Point two, safety is the absolute number one priority.

These drugs have incredibly narrow therapeutic windows.

The difference between healed and harmed is a few decimal points on a lab result.

Know your levels.

Point six to one point two for lithium.

Memorize it.

Point three,

patient education is your most powerful tool.

You can't be with the patient Tumor 47.

They have to be your partner in their own safety.

They need to know about the water, the salt, the rash, the tremor.

You have to empower them to be safe.

And point four, the nurse's role.

It's all about monitoring.

It's about being a detective.

It's noticing the coarse tremor before the seizure happens.

It's noticing that the patient is saying, I'm just a little thirsty before their lithium level hits 2 .5.

It's checking the platelets and the white blood cells and connecting the dots between a sore throat and a potentially fatal drug reaction.

It really highlights that psychiatric nursing is not just about talking to people about their feelings.

It is hardcore physiology and pharmacology.

Absolutely.

You are managing a complex biological system that is under assault from both the illness itself and sometimes from the cure.

I want to leave our listeners with a final provocative thought that comes from the text.

It mentions this idea of sub -threshold symptoms.

Ah, yes.

This is really the frontier of treatment.

These are symptoms that aren't quite clinical, meaning they don't meet the full DSM criteria for a manic or depressive episode, but they still affect the person's life.

A little irritability, slight changes in sleep, shifts in energy.

We've gotten good at stopping the hospitalization.

We can usually stop the full -blown mania, but can we give the person their nuance back?

Can we get them back to feeling truly consistently well?

And it really asks us to consider how much of what we call personality is actually biology and how fine is that line the nurse walks in, helping a patient return to themselves without dulling the spark that makes them who they are.

That is the art of nursing, isn't it?

The science is the lithium level.

The art is helping Bill or Johnny or any patient live a life that feels worth living while they're on these powerful medications.

Because if they don't like the life they have on the drug, they won't take the drug.

And then the whole cycle just starts all over again.

Well said.

Thank you so much for joining us for this deep dive into Chapter 16.

My pleasure.

It was great.

Good luck with your studies.

Keep your sodium study.

And a warm thank you from the last -minute lecture team.

We'll see you next time.