Chapter 14: Antipsychotic Drugs: Uses & Effects

Welcome to Last Minute Lecture.

This free chapter overview is designed to help students review and understand key concepts.

These summaries supplement not replaced the original textbook and may not be redistributed or resold.

For complete coverage, always consult the official text.

Welcome back to the Deep Dive.

Today we are opening up a file that, and this is no exaggeration, sits right at the intersection of some really hardcore neurochemistry and

the most profound and sometimes terrifying human experiences.

We are tackling chapter 14 of psychiatric nursing and the topic is anti -psychotic drugs.

This is a heavy chapter, and I don't just mean heavy in terms of the molecular biology, which is dense.

It's heavy in terms of the history and the impact these medications have had.

These are the medications that quite literally tore down the walls of the asylums.

It's so easy to forget that, isn't it?

We see a pill bottle today and we just think, okay, that's standard treatment.

But the text, it sets the stage with this really stark contrast between the then and the now.

It does.

And to really grasp why this chapter matters so much, you absolutely have to look at Norm's notes, you know, those introductory thoughts from the author.

He takes us back to the era before 1950.

The pre -Thorazine days.

Exactly.

He calls it a madhouse and he's not being figurative.

No, not at all.

He means it literally a house of madness.

He does.

He describes the state hospitals of the 1930s and 40s as just places filled with absolute pain and agony.

I think it's so important for the nursing students listening to really visualize this.

Before we had these drugs, we didn't have treatment.

We had containment.

That's the perfect word for it.

Containment.

The text even mentions isolation, physical restraints for days, maybe weeks on end.

And it got worse.

The things they did because there was just no chemical way to calm the storm in the brain.

So they turned to psychosurgery.

We're talking about lobotomies.

Yeah.

And we're talking about things like hydrotherapy, which sounds kind of nice and spa -like, but it was actually wrapping people in freezing cold wet sheets for hours.

To shock them into submission.

Exactly.

It's just, it's a horror movie scenario.

And the text makes this chilling point.

When a patient was admitted back then, there was basically zero expectation that they It was a life sentence.

It was.

The backwards of these hospitals were essentially warehouses for the forgotten.

But then 1950 rolls around and we get what I consider one of the greatest happy accidents in all of medical history.

I love these stories.

It's like science just stumbling into a miracle.

So nobody was actually trying to cure schizophrenia in 1950.

Not even close.

There was a French scientist and he was trying to develop a new antihistamine for allergies or maybe to use as a sedative for surgery.

Right.

And he synthesized this compound called chlorpromazine.

Which we all know today is thorazine.

That's the one.

And at first they used it for presurgery jitters, just to calm people down before they went under the knife.

But the doctors, they started observing these patients and they noticed something profound.

It wasn't just that they were sleepy.

No, it was more than that.

It was that they were

indifferent.

Indifferent to the chaos to the surgery.

Indifferent to their psychosis.

The hallucinations might still have been there, but they lost their emotional power.

The delusions stopped driving the behavior.

It fundamentally altered the psychotic state.

And just like that, thorazine became the first true antipsychotic drug.

And that just changed everything.

It emptied the hospitals.

I mean, suddenly patients who had been screaming in for five years were calm.

They could talk.

They could dress themselves.

They could actually go home.

It was the penicillin moment for psychiatry.

So let's fast forward to today.

The text mentions that spending on these drugs in the U .S.

is something like, what, $16 .1 billion a year?

It's a massive industry.

Absolutely massive.

These are consistently among the top selling drugs in the world.

But are we just treating schizophrenia with that $16 billion?

Or has the use expanded?

Well, schizophrenia is the core indication for sure.

Schizophrenia, Schizoaffective disorder, and the manic phase of bipolar disorder.

But you're right.

The scope has really crept outward.

The text lists a whole host of off -label uses.

Off -label meaning,

the FDA didn't technically approve it for that, but doctors know it works.

Precisely.

You'll see antipsychotics prescribed for severe insomnia, for ticks like in Tourette's, for delirium in the ICU.

And I found this fascinating, even for stuttering sometimes.

Okay, so our mission for this deep dive is pretty clear then.

We have a lot of nursing students listening who are probably staring at this chapter terrified of the pharmacology.

I get it.

It's intimidating.

So we need to take all this complex chemistry and translate it into

survival skills.

That's it.

We need to move beyond just memorizing long lists of side effects.

We need to understand the logic of the system.

Because if you understand the mechanism, you don't have to memorize the side effects.

You can predict them.

You can predict them.

Exactly.

All right.

Let's start with the landscape.

The text breaks these drugs down into two big families.

You've got the old guard and the new school.

Right.

If you're following along, this is table 14 to one in your text.

You have the traditional antipsychotics.

You'll also hear them called first generation or typical.

These are the drugs developed between 1950 and 1990.

So Thorazine, Haldol, those guys.

And then you've got the atypical or second generation drugs, which started showing up around 1990.

Correct.

But before we get into the new stuff, we have to nail down a concept that trips up almost every student I've ever taught.

And that's the concept of potency in those traditional drugs.

Yeah.

Let's unpack this.

Because when I see the term high potency, my brain immediately goes to better.

Like, you know, high potency detergent cleans your clothes better.

Yeah.

And that is the trap.

One hundred percent.

In this specific area of pharmacology, potency has zero to do with clinical efficacy.

Let me say that again.

High potency does not mean works better.

So what does it mean?

It strictly refers to the milligram dosage you need to get the job done.

Okay.

Give me a real world comparison because the text talks about milligrams, but it's hard to visualize what that means in the body.

Okay.

Think of it like alcohol.

Let's compare a light beer to, say, Everclear or 151 proof rum.

Okay.

I'm with you.

If your goal is to get legally intoxicated, let's call that the clinical effect.

You can do it with a light beer or you can do it with the Everclear.

The end result is exactly the same.

You're drunk, but the process of getting there is very different.

Totally different with the light beer.

That's your low potency drug like you have to drink a lot of liquid, you know, maybe six cans in drug terms.

We're talking a hundred milligrams, 200 milligrams, sometimes more.

That's a lot of physical substance circulating in your body.

And because there's so much of that stuff floating around, it bumps into everything.

It's not very specific.

It hits your blood pressure receptors.

It hits your gut receptors.

It causes a lot of sedation.

So low potency drugs have a really messy side effect profile when it you get really sleepy.

So bigger pill, more body collateral damage.

That's a great way to put it.

Now look at the Everclear.

That's your high potency drug like Haloperidol, which is Haldol.

You only need a tiny drop, a single shot to get the same level of intoxication.

In drug terms, that's maybe two milligrams or five milligrams.

So way less liquid, less body side effects.

Exactly.

Yeah.

You see way less sedation and much less low blood pressure because there isn't as much drug just flooding the entire system.

But, and this is the huge but, because that tiny amount is so concentrated and it hits the brain receptors so hard.

It hits the brain like a sledgehammer.

Precisely.

So you trade the body side effects for brain side effects.

High potency drugs are the ones that cause the rigid muscles, the tremors, that classic zombie look.

These are the EPSEs, the extra -paramidal side effects.

So it really is a trade off.

You're literally choosing your poison.

No.

Do you want the patient to be dizzy and sleepy, which is low potency, or do you want to risk them locking up like the Tin Man from the Wizard of Oz, which is high potency?

That is the clinical decision making process in a nutshell.

And for you as the nurse, knowing the potency tells you exactly what to watch for.

If I give a dose of Thorazine, I'm watching that blood pressure cuff.

If I give Haldol, I'm watching the patient's hands for tremors.

That makes it stick.

Okay.

Now we've alluded to dopamine a few times.

To really understand why these drugs work, and just as importantly, why they cause these very specific side effects, we have to go deep into the brain.

The text calls this the neurochemical theory.

This is the bedrock.

For decades, the prevailing theory has been the dopamine theory.

And put simply, it's this.

Schizophrenia looks like too much dopamine in specific parts of the brain.

So the antipsychotic is basically the brake pedal for dopamine.

Yes.

These drugs are antagonists.

They block the D2 dopamine receptor.

Think of the receptor as a parking spot.

The drug pulls a car into that spot so the dopamine can't get in and park.

But the brain isn't just one big bucket of dopamine, right?

It has highways.

And this is the most important part of the chapter.

It's figure 14 to one in the text, which outlines the four dopaminergic tracts.

I call them the four highways.

If you can memorize these four highways, I promise you, you will understand everything about how these drugs work.

All right, let's drive down them.

Highway number one.

That's the mesolimic tract.

This is the scenic route, the one involved in emotion, memory, sensory processing.

In a person with schizophrenia, this highway is jammed with traffic.

Just way too much dopamine.

And that traffic jam is what manifests as?

The positive symptoms, the hallucinations, hearing voices, the delusions, the paranoia.

The brain is just overfiring.

So when we give an antipsychotic, we put up a roadblock.

We block the dopamine receptors on that highway.

The traffic clears up and the voices stop.

This is the therapeutic effect.

This is exactly what we want the drug to do.

Perfect.

Mission accomplished.

But the drug travels through the entire blood supply.

It doesn't have a little GPS that says, hey, only go to the mesolimic tract.

And that is the tragedy of the traditional antipsychotics.

They are incredibly blunt instruments.

They block dopamine everywhere.

Which brings us to highway number two, the negrostriatal tract.

Okay, what does this highway control?

This one connects the decision to move with the actual movement.

It's the motor control center.

In a healthy person, dopamine is like the grease in the gears.

It's what makes movement smooth and fluid.

But we just swallowed a massive dose of Haldol to stop the voices on highway one.

And that same dose of Haldol flows right onto highway two and sets up the exact same roadblock there.

It strips all the grease out of the gears.

So the traffic stops.

The movement stops.

Total gridlock.

This is why patients on these drugs develop Parkinsonian symptoms.

Parkinson's disease is literally a lack of dopamine in this specific tract.

We are chemically inducing Parkinson's disease to cure their psychosis.

That is heavy.

You're trading insanity for physical rigidity.

It's a very, very steep price to pay.

And it's why so many patients hate taking these medications and stop.

Okay.

Highway number three.

The tuberoin -fundibular tract.

This little highway goes to the pituitary gland.

Now, normally dopamine acts as a specific inhibitor here.

It tells the body, do not make prolactin, which is the hormone for breast milk.

So if we block the dopamine.

We lift that inhibition, the break is gone.

The body thinks, oh, I guess it's time to lactate.

So prolactin levels in the blood to spike.

So you can have men developing breasts, which is called gynecomastia, and women who aren't pregnant are breastfeeding, suddenly producing milk.

Exactly.

Again, a massive quality of life issue leads to nonadherence.

And finally, highway number four, the mesocortical tract.

This is the highway for executive function, thinking, planning,

motivation, problem solving.

Now here is where it gets really tricky.

In schizophrenia, while the emotional center has too much dopamine, this thinking center might actually has too little to begin with.

So the highway is already kind of empty?

It's barren.

And that's what we think causes the negative symptoms, the lack of the abolition, the flat affect, the social withdrawal.

Wait a second.

If there's already too little dopamine there and we give a drug that blocks what little dopamine is left.

We make it worse.

We turn a quiet highway into a complete dead zone.

And this is why traditional drugs like Thorazine and Haldol are great at stopping the voices, but they can lead the patient feeling like a zombie, totally unmotivated and emotionally flat.

This sounds like a fundamentally flawed system.

We're fixing one problem, but we're actively causing three others.

Which is exactly why the pharmaceutical industry spent billions of dollars developing the atypical antipsychotics.

The new school, the text calls this the atypical advantage.

But I have to challenge this a bit.

You just told me that an antipsychotic is a dopamine blocker.

And you told me that blocking dopamine causes movement disorders.

So how can a drug be an antipsychotic and not cause movement disorders?

Is it magic?

It's a little bit of biochemical magic.

Yes.

It's the dual action theory, which you can see in figure 14 to two.

Okay, break it down for me.

So atypicals like risperdal or zyprexa, they block dopamine.

Yes.

But they also block serotonin receptors,

specifically a receptor called 5 -HT2A.

Okay.

So you're bringing a second player into the game now.

What does blocking serotonin do?

It turns out that serotonin and dopamine have this

t -tauter relationship in certain parts of the brain.

If you block serotonin in the tract,

that's the movement highway.

Remember blocking serotonin there actually causes dopamine to be released.

Whoa.

So the drug is blocking dopamine with one hand, but it's blocking serotonin with the other, which in turn causes the brain to release more dopamine.

Exactly.

So in the limbic system where the voices are, the dopamine blockade wins.

The psychosis gets better.

But in the movement center, that serotonin blockade releases just enough dopamine to compete with the drug.

It sort of creates a wash.

It balances it out.

Ideally, yes.

Yeah.

It creates just enough dopamine flow to keep the muscles moving smoothly.

You get the anti -psychotic effect without the Parkinson's effect.

It's brilliant.

That is brilliant.

And there's another theory too.

It's called the fast -off theory.

What's that about?

Traditional drugs like Haldol are like a sticky guest at a party.

They sit on that D2 receptor and they just refuse to leave.

Atypicals are fast -off.

They bind to the receptor, do their job for a second, and then they jump off quickly.

This rapid dissociation gives the brain's natural dopamine a chance to still work, which further reduces those rigid side effects.

Okay.

So with all that, atypicals seem like the clear winner.

Why do we even use the old ones anymore?

Because, as we're going to see in a bit, atypicals traded the movement problem for a metabolic problem.

There is no free lunch in pharmacology, ever.

All right.

Let's pivot to the symptoms themselves.

We've been tossing around the terms positive and negative symptoms.

Box 14 -4 in the book breaks this down.

This terminology always felt a little backward to me.

I mean, positive usually means good, right?

Chuckles.

Yeah, it's confusing.

In medicine, positive just means present.

They give it like math.

You are adding something to the patient's reality that shouldn't be there.

So a hallucination is a plus that's been added.

Yeah, exactly.

Delusions, agitation, bizarre patterns of speech.

These are positive symptoms, and they're caused by that dopamine flood in the mesolimbic tract.

And the good news is, pretty much all antipsychotics are really good at scrubbing these away.

So negative must mean?

Subtraction.

Something is missing.

The patient has lost their motivation.

That's abolition.

They've lost their ability to feel pleasure and hedonia.

They've lost their facial expressions, blunted affect.

And as we just discussed, the traditional drugs are terrible at fixing these.

They often make them worse, unfortunately.

And this is why if you have a young patient who needs to go back to college or hold down a job, you really want to lean toward using the atypicals.

They address those negative symptoms much better by sparing the dopamine in the cortex.

I want to ask about the timeline.

For years, we used to call these drugs major tranquilizers.

Oh, that's a very dated term, yeah.

But it implies they work instantly.

If I take a Tylenol, my headache is gone in 30 minutes.

Is it the same here?

That's a great question.

And it's yes and no.

And this is vital for nursing education.

If you give a shot of Haldol to a really agitated patient, they will calm down in about 30 to 60 minutes.

That is the sedative effect.

Okay.

So that part is fast.

That part is fast.

But the actual antipsychotic effect, the disappearance of the delusion that the CIA has planted a chip in their brain, that takes weeks, usually three to six weeks, sometimes even longer.

Why the lag though?

I don't get it.

If the receptor is blocked today, why isn't the delusion gone today?

That's sort of the million dollar question.

The theory is that the brain needs time to structurally adapt.

It needs to rewire itself around this new chemical reality.

So it's crucial for nurses to teach families this.

You have to say, look, dad isn't going to wake up cured tomorrow morning.

We need to be patient with this process.

That's a huge teaching point.

Okay.

Let's move on to section four.

Pharmacokinetics, or as I like to call it, the invisible traps.

Chuckles.

There are some massive traps here for new nurses.

The first one involves fat.

Right.

These drugs are lipid soluble.

ILY.

They love fat.

They ignore water and they just soak right into the adipose tissue.

They basically hibernate there for a long time.

The text tells the story of Bob.

And I think Bob's story is something that every single nurse will see in real life at some point.

Oh, absolutely.

Bob is a classic case.

He's been on HowlDoll for decades.

He's stable, but he gets tired of the side effects, you know, or maybe he just wants to feel natural again.

So he decides to quit cold turkey.

I can do this on my own.

Mind over matter.

Right.

And here's the trap.

Monday comes, he feels fine.

Wednesday comes, he feels great.

He's clearer.

He's telling the staff, see, you're all wrong.

I didn't need those pills.

And a novice nurse might be thinking, hey, you know what, maybe he's right.

Exactly.

Week one goes by.

Week two, Bob is doing great.

But what he doesn't realize is that he's living on borrowed time.

He's running on a battery.

He's running on a fat battery.

His body fat is slowly leeching that stored HowlDoll back into his blood and is keeping his levels therapeutic.

But around week three or maybe week four, the battery dies.

The stores run dry and Bob crashes and he crashes hard.

The psychosis returns with a vengeance.

So the lesson for nurses is non -inherence doesn't show up immediately.

Just because a patient looks good a week after they stop their meds doesn't mean they are safe.

Okay.

Trap number two, cigarettes.

I honestly had no idea about this one until I read this chapter.

It's fascinating.

This is the woodshipper scenario.

Yeah.

It all comes down to a liver enzyme called CYP450 -1A2.

Catchy name.

I know, right?

But here's the deal.

The hydrocarbons and cigarette smoke, and it's the smoke itself, not the nicotine.

They rev up this enzyme.

They basically turn it into a high -speed woodshipper for certain drugs, specifically clozapine and olanzapine.

So if you smoke, your liver is just chewing up the drug really, really fast.

As fast as it can.

Yeah.

A heavy smoker might need double the dose of a non -smoker just to get the same clinical effect.

So here's the nursing trap.

Walk me through how this goes wrong on a unit.

Okay.

So you admit a patient from home.

He smokes two packs a day,

but your hospital is a smoke -free facility, of course.

So he has to use nicotine patches.

So there's no smoke.

No smoke.

Which means that woodshipper enzyme in his liver goes to sleep.

It slows way down.

Now the doctor starts him on olanzapine.

They find a dose that works, let's say it's 10 milligram.

He stabilizes.

He's discharged.

And on the way to the parking lot.

He lights up a cigarette and he goes right back to his two pack a day habit.

Within a couple of days, that liver enzyme wakes up and starts shredding that olanzapine at high speed.

So his 10 milligram dose effectively becomes a five milligram dose.

Or less.

And he relapses.

He ends up right back in the ER and everyone on the team is scratching their head saying, oh, the drug just stopped working.

No.

The environment changed the metabolism.

Nurses have to be hyper aware of smoking status, both on admission and a discharge.

That is wild.

Last trap in this section.

Checking.

This is more of a behavioral trap than a chemical one.

Patients, especially paranoid ones, will hide pills in their cheeks to spit out later when no one's looking.

Why do they do that?

Is it just being difficult or oppositional?

We have to have some empathy here.

Imagine the side effects we just described.

The dry mouth, the rigidity, the sexual dysfunction, the weight gain.

Would you want to take that pill every day?

For many patients, they feel like they're being poisoned.

Cheeking is a survival strategy for them.

But obviously they need the medication to stay well.

So what's the fix for that?

Well, liquid concentrates are one option.

You can't really cheek a liquid, but the gold standard solution these days is the depo.

The long acting injectable.

Right.

Drugs like haloperidol decanoate or invega cistena.

You give an injection into the gluteal muscle once every two weeks or even once a month.

And it just takes that daily battle completely out of the equation.

It does.

It protects the patient from their own forgetfulness or their ambivalence about treatment.

And for many people, it is the difference between a revolving door admission cycle and living a stable, productive life in the community.

Let's move to section five, side effects.

The text calls this the cost of treatment, which feels right.

We've touched on some of them, but let's systematize this for the students.

First, the PNS effects, the body stuff.

This is mostly anti -colonergic effects.

We're blocking the cranial nerves.

So dry mouth is a big one.

Dry mouth, dry eyes, constipation is a huge one.

That's the vagus nerve, cranial nerve X being blocked.

And the text has a specific alert here for older men.

Yes.

Urinary retention.

If a man already has an enlarged prostate and you give him a drug that clamps down on the bladder sphincter, he can't pee.

And that can quickly become a medical emergency.

Then there's Ulthostatic hypotension.

This is the anti -adrenergic effect.

The blood vessels lose their ability to constrict when you stand up.

So gravity wins.

All the blood pools in your legs, your brain doesn't get enough oxygen and you get dizzy or even faint.

And nursing intervention there is?

Safety, safety, safety.

Teach them to dangle, sit on the edge of the bed for a full minute before you try to stand up, let your body adjust.

Okay.

Now for the big ones, the ones everyone is scared of, the EPSEs, the extra pyramidal side effects.

We know the dopamine blockade in the motor track causes these, but they come in different flavors.

They do.

And it's critical to know the difference because you treat them differently.

First up is akathisia.

The text calls this subjective restlessness, which sounds pretty mild.

It is not mild.

That's way too polite.

Patients describe it as jumping out of my skin.

It's a feeling of internal torture.

Ants in the pants,

they cannot sit still.

It will pace back and forth for hours.

And this is dangerous because?

It looks exactly like agitation.

A nurse sees a patient pacing and thinks, oh, his psychosis is getting worse.

I should give him more Haldol.

Which is just pouring gasoline on the fire.

Exactly.

More Haldol equals more akathisia.

The correct treatment is to lower the dose of the antipsychotic or maybe give a beta blocker like propranolol.

Next is dystonia.

This one sounds terrifying just from the name.

This is freezing.

It's a sudden, severe, and very painful muscle cramp.

Usually it affects the head and neck.

You might see torticollis, where the head twists to the side and just locks there.

Or the oculodgeric crisis.

Yes, where the muscles that control the eye go into spasm and the eyes roll back into the head and get stuck there.

I mean, imagine how terrifying that is.

You can't look down.

You're just stuck staring at the ceiling.

And the most dangerous one is laryngeal dystonia.

The throat muscle spasm.

It cuts off the airway.

This is a call 9 -1 -1 or call the code team moment.

It's a true emergency.

Is there an antidote?

Thankfully, yes.

Anticholinergics.

A shot of benztropine, which is cooked gentin, or even just benadryl.

It works almost instantly.

It's like a key that unlocks the muscles.

Then we have Parkinsonism, which we've already discussed.

The tremors, the shuffling gait, the rigidity.

And finally, the absolute tragedy of tardive dyskinesia.

TD.

Tardive means lid appearing, right?

Yes.

This is something that happens after years of treatment.

The dopamine receptors become hypersensitive from being blotched for so long.

And you start to see these bizarre involuntary facial movements.

Lips smacking, tongue writhing, constant chewing motions.

And the tragedy of it is.

It's often prominent.

Even if you stop the drug, the tongue keeps moving.

It's incredibly stigmatizing.

That's why we have to screen for it constantly using the AIM scale.

The Abnormal Involuntary Movement Scale.

Prevention is everything.

Okay.

We have two big syndromes to cover now.

One that tells you fast and one that kills you slow.

Let's do the fast one first.

Neuroleptic Malignant Syndrome or NMS.

This is rare.

Maybe affects 1 % of patients, but it is absolutely fatal if it's missed.

What are the cardinal signs?

What are the red flags we look for?

Rigidity and heat.

The patient becomes stiff as a board.

Lead pipe rigidity.

And there are temperature spikes.

We're talking 103, 105,

sometimes even 108 degrees Fahrenheit.

It literally cooks the brain.

Essentially, yes.

The autonomic nervous system completely collapses.

So the action plan for the nurse?

Stop the antipsychotic immediately.

Do not pass go.

Do not collect $200.

Stop the drug.

Then you cool the patient down ice packs in the armpits and

groin cooling blankets.

You hydrate them with IV fluids.

This is usually an ICU transfer.

Okay.

That's the fast killer.

Now for the slow killer.

Metabolic syndrome.

This is the curse of the atypicals.

This is the trade -off we talked about.

We fixed the movement problems, but we broke the metabolism.

Drugs like Alanzapine, Cyprexa, and Clozapine, Clozrol fundamentally change how the body processes sugar and fat.

The text mentions a patient named Bud.

Bud's story is heartbreaking.

He gained 105 pounds in one year.

Just imagine the physical strain of carrying an entire extra person on your back every single day.

That's heart disease waiting to happen.

That's joint pain.

That's diabetes.

It's full -blown metabolic syndrome.

High blood pressure.

High triglycerides.

Fasting blood sugar.

We are in effect giving these patients type 2 diabetes with these medications.

So the nurse needs to be bringing a tape measure to the appointment, not just a blood pressure cuff.

Absolutely.

Wazirconference is a vital sign in psychiatry now.

If we see that weight shooting up or the waistline expanding, we have to intervene.

We might need to switch them to a more weight neutral drug like Abilify or Geodun.

Okay.

Let's do the roll call.

We've dropped a lot of drug names.

Let's create a quick yearbook for these drugs so the students can keep them straight.

This is section 6.

Sounds good.

Let's start with the classic traditionals.

First up, Thorazine.

Chlorpromazine.

The grandfather of them all.

Low potency.

Just think Sledgehammer of sedation.

Causes a ton of weight gain and low blood pressure.

It's rarely used for psychosis anymore, but you might still see it for intractable hiccups or severe nausea in cancer patients.

Okay.

Haldol.

Halperidol.

The high potency king.

Very little sedation, but a huge, huge risk of muscle cramping and stiffening the EPSEs.

It's still often used in the chemical restraint cocktail Haldol plus Ativan for acutely aggressive patients because it works fast and you can inject it.

All right.

Let's move to the atypicals.

The first one is Clozapine.

Closerol.

Ah, the Diva.

It is without a doubt the most effective drug we have for schizophrenia.

It works for patients who have failed every other medication.

It's the only one proven to reduce suicide risk.

But the Diva has demands, doesn't she?

She has huge demands.

It causes a life -threatening side effect called granulocytosis.

It suppresses the bone marrow so your body stops making white blood cells.

So a common cold or a sore throat could actually kill you?

Yes.

And that's why there's a national registry for this drug.

You cannot get a prescription for Clozapine without a blood test showing that your white blood cell count is safe.

The text mentions a clinical story about Joan.

She gained 40 pounds on Clozapine.

She hated the weekly blood draws.

But she absolutely refused to stop taking it.

Because for the first time in her life, the voices were quiet.

She could hold down her job.

It really puts that side effect trade off into a very human perspective.

Okay.

Next up, Risperdal.

Risperidone.

Risperdal is the in -between drug.

It's classified as an atypical.

But at higher doses, it starts to act like a traditional drug and causes a lot of movement problems.

It's also the worst offender for raising prolactin levels.

That's the breast milk issue we talked about.

Exactly.

What about Zyprexa, Alanzapine?

The heavyweight champ.

It is incredibly effective.

Very calming for agitated patients.

But the weight gain is legendary.

That's the bud drug.

The one where he gained 105 pounds.

The risk of metabolic syndrome is extremely high.

Okay.

Seroqual, K -chipine.

The baby heroin.

That's its street name.

Baby heroin.

Why?

Because it's heavily sedating.

In prisons and on the street, it's abused because it helps people just sleep away their sentence or their problems.

Clinically, we use it when that sedation is desired, like for a patient with insomnia.

But we have to be very watchful for abuse potential.

Geothalon.

Depressidone.

What do we need to know here?

Two things.

One, you have to take it with food.

At least 500 calories.

If you don't, the body barely absorbs it.

Two, it can stretch out the QTC interval on an EKG.

Which is a risk for a fatal heart arrhythmia.

It's rare, but it's a real risk.

So you should get a baseline EKG before starting it.

And finally, the last big one.

Abilify.

Erpiprazole.

I call this one the Goldilocks drug.

It's not just a blocker.

It's a dopamine system stabilizer.

It's a partial agonist.

So if dopamine is too high in one brain area, it brings it down.

But if it's too low in another area, it actually brings it up.

So it's just right.

Less side effects.

Generally, yes.

Much less weight gain, less sedation.

It's very popular for that reason.

But for some patients, it can cause that inner restlessness.

The akathisia we talked about.

Let's move to section seven.

Nursing considerations.

We've covered a lot of the specifics, but let's just hit the general safety rules for the whole class of drugs.

Okay.

First and foremost, CNS depression.

These drugs slow the brain down.

If you mix them with alcohol or opioids or barbiturates, you could have an additive effect and actually stop the breathing drive.

It's a dangerous combination.

What about pregnancy?

They all cross the placenta.

It's always a risk -benefit discussion with the patient and her doctor.

But generally, we try to avoid them in the first trimester, if at all possible.

And the black box warning for the elderly.

This is a big one.

This is crucial for anyone working in geriatrics.

Do not use antipsychotics to treat wandering or general confusion in patients with dementia.

It has been shown to increase the risk of death from stroke or pneumonia in this population.

Finally, patient teaching.

If I'm a new nurse sending a patient home on one of these for the first time, what are the top tips I absolutely have to tell them?

Okay.

Four things.

Number one, sunscreen.

These drugs cause severe photosensitivity.

You will burn instantly.

Heat safety.

You can't regulate your body temperature properly on these drugs.

So no hot tubs, no running marathons in July.

You are at very high risk for heat stroke.

Report any sign of infection,

a sore throat,

a fever.

You call us immediately.

It could be a sign of a granulocytosis.

And number four, never ever stop abruptly.

The rebound psychosis can be severe.

Let's wrap this up with a quick look at the future.

We've been obsessed with dopamine for this entire deep dive.

Is there anything else on the horizon?

There is.

It's called the glutamate hypothesis.

We know from experience that drugs like PCP and ketamine, which block a neurotransmitter called glutamate, can cause symptoms that look almost exactly like schizophrenia.

Which suggests that glutamate must be a big player in the disease too.

That's the idea.

The hope is that the next generation of drugs might target the glutamate system.

And if we can fix that system, we might finally be able to effectively treat the cognitive decline and the negative symptoms that our current dopamine -focused drugs just can't touch.

It really feels like we are just scratching the surface of the brain's complexity.

Oh, we are.

But when you compare it to the madhouse of 1940, with the restraints and the lobotomies, we've come a very, very long way.

This has been a massive deep dive.

We went from the ever -clear potency analogy all the way down to the traffic jams on the four brain highways.

Yeah, we looked at those tragic trade -offs, you know, sanity versus virginity or clarity versus obesity.

And we highlighted all those invisible traps for the new nurse.

The fat storage, the cigarette smoke, the cheeking.

And I think most importantly, we highlighted the role of the nurse in all of this.

You are the one who is going to notice that first little hand tremor.

You are the one who is going to measure the waistline and see it expanding.

You are the one who has to explain to the family why dad isn't better in 24 hours.

You are the bridge between the molecule and the person.

That's beautifully said.

That's exactly it.

Thank you for listening to this deep dive.

Warm regards from the Last Minute Lecture Team.

Now go ace that exam.