Chapter 13: Antiparkinsonian Drugs in Mental Health Care

Welcome to Last Minute Lecture.

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

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

For complete coverage, always consult the official text.

Welcome back to another Deep Dive.

We are so glad you're here with us.

It's good to be back.

Today we are pulling apart a topic that, um, on the surface looks like it belongs in a neurology ward, not really a psychiatric one.

We are digging into Chapter 13 of Psychiatric Nursing, the seventh edition.

And the chapter title is simply Anti -Parkinsonian Drugs.

And that title, it really throws a lot of nursing students off.

I see it all the time.

How so?

Well, you see anti -Parkinsonian and you immediately think, okay, we're treating Parkinson's disease, grandpa's shaky hands.

And look, while that is technically true in a, you know, a very broad medical sense, in the world of psychiatric nursing, this chapter is actually about something much more specific and frankly, a bit more ironic.

Ironic.

I'm intrigued.

What's the irony?

The irony is that the real meat of this chapter, the reason we are spending a whole deep dive on it, isn't about treating an organic disease.

It's about cleaning up a mess that we made.

We made, as in the clinicians.

Exactly.

We're talking about the side effects of anti -psychotic medications.

We give drugs to treat psychosis, to quiet the voices, and in the process, those very same drugs can break the movement centers of the brain.

So this chapter, these drugs,

they're the cleanup crew.

Wow.

That is, that's a hell of a way to frame it.

So we are not just memorizing a list of drugs today.

This is not a simple pharmacology review.

Definitely not.

If you just memorize the list, cogentin, artane, benadryl, you'll be dangerous on the floor.

You absolutely have to understand the mechanism behind it all.

So what's the mission today?

The mission is to decode this whole process.

We're talking about extra -paramidol side effects, or EPSEs.

If you're a student listening to this, this is incredibly high -yield stuff for exams.

And if you're already a working nurse.

This is what keeps your patients safe.

This is what separates a good nurse from a great nurse, spotting these things early.

And you know, if you're just curious about how the brain works, this is a fascinating, if slightly terrifying, look at how delicate our chemical balance really is.

I love that.

Okay, so we're going to follow the chapter's roadmap.

We'll start with the biology of movement, the neurotransmitters.

Then we'll figure out why treating schizophrenia makes people shake.

Then we hit the drugs we use to fix it, the anticholinergics and all the nursing implications that come with them.

Perfect.

But before we get into the heavy chemistry, let's set the stage because the book makes a really big distinction right at the start.

It separates Parkinson's disease with a capital P from Parkinsonism with a lowercase P.

A huge distinction.

You have to get this right from the jump.

Parkinson's disease, PD, is a progressive, chronic, degenerative disease of the brain.

Degenerative meaning cells are dying.

Cells are dying.

The text says it has an unknown cause, though we know where the damage is happening.

And it's common.

It's affecting about 1 % of the population over age 60.

And it's not cheap.

The text puts a price tag on it for the U .S.

economy.

A big one, roughly $2 billion annually.

Think about the loss productivity, the cost of care, the medications.

It's a massive burden on the health care system and, of course, on families.

So that's the disease.

That's organic neurodegeneration.

Correct.

But what we're usually dealing with in psychiatry is Parkinsonism, lowercase P.

And the thing is, it looks the same.

The tremors, the shuffling gait, the rigid, mask -like face.

It's a mirror image.

But the cause is completely different.

Completely.

If I walk onto a psych unit and see a 25 -year -old man shuffling down the hall, his arms frozen at his sides, his face expressionless, he doesn't have the degenerative disease of a 70 -year -old.

No, almost certainly not.

He has drug -induced Parkinsonism.

We gave him an anti -psychotic, maybe Haldol or Thorazine, to treat his hallucinations.

And that drug blocked the dopamine receptors in his brain so effectively that it mimicked the exact symptoms of Parkinson's disease.

That is the core tension here, isn't it?

This is the fundamental conflict of the chapter.

Treating the mind can freeze the body.

That's it in a nutshell.

So to understand why that happens, why we can't seem to just treat the voices without wrecking movement, we have to look under the hood.

We need to talk about what the book calls the extrapyramidal system.

Now, just the name sounds intimidating.

It does.

It sounds like ancient architecture or something from a geometry textbook, but it's really just a functional area of the brain.

It's not one single structure.

Okay, so what does it do?

The text defines the extrapyramidal system as the area responsible for the coordination of involuntary movement, which supports voluntary movement.

Untack that.

Involuntary supporting voluntary.

That sounds like a contradiction.

It does, but think about it like this.

When you decide to walk down the street to grab a coffee, the act of walking is voluntary.

You are consciously commanding your legs to move forward.

Right.

I'm in control.

But are you consciously commanding your arms to swing in perfect rhythm with your legs?

No, that just happens.

Are you commanding the dozens of tiny muscles in your back and core to make constant micro adjustments so you don't tip over on an uneven sidewalk?

Absolutely not.

I'd fall over if I had to think about that.

Exactly.

That's the extrapyramidal system.

It's the autopilot.

It's the suspension in your car.

It handles all the smooth, coordinated background movements that make your main voluntary movements

It provides the fluid framework.

So when that system crashes?

The autopilot is offline, and your voluntary movements become jagged, difficult, rigid, or even impossible.

And the text gives us the cardinal symptoms of when this system goes offline.

It calls them the big four.

The big four.

If you're a nursing student, tattoo these on your brain.

If you see these, you know the extrapyramidal system is in trouble.

Number one, tremors.

The classic shaking.

Usually resting tremors.

It's often that pill -rolling motion of the fingers and thumb as if they're rolling a small pill back and forth.

It happens when the hand is at rest.

Okay, what's number two?

Number two is bradykinesia.

Which is Latin for?

Slow movement.

Brady means slow, kinesia means movement.

But it's more than just being sluggish, it's a profound difficulty initiating movement.

The signal from the brain to the muscle seems to get stuck.

So the patient might look like they're hesitating before they stand up.

Or they might freeze mid -stride.

It's a visible struggle to get the body to obey.

Okay.

Tremors, bradykinesia.

Number three.

Rigidity.

The muscles are just tight and flexible.

You might feel it if you try to move a patient's arm.

It's like trying to bend a lead pipe.

It's a sustained resistance.

And the last of the big four.

Postural instability.

This is why these patients have such a high fall risk.

Those micro adjustments we talked about, the ones that keep you balanced, they're gone.

So they're easily knocked off balance and can't correct themselves.

They often have that shuffling stooped over gait.

Tremors, bradykinesia, rigidity, instability.

Got it.

Now, what's fueling this system?

What's the gas in the tank, chemically speaking?

The text introduces two main neurotransmitters and they use a visual that I found really, really helpful.

The seesaw.

The seesaw.

It's so simple, but it explains everything.

It really does.

Figure 13 to 3 in the text literally shows a seesaw.

On one end, you have a little figure labeled dopamine.

On the other end, a figure labeled acetylcholine, or AC for short.

OK, so let's unpack the seesaw.

What are the roles of these two chemicals?

For you to move smoothly, to pick up this cup of coffee without spilling it, that seesaw needs to be perfectly level.

Dopamine and acetylcholine have to be in balance, but they have opposite jobs.

Dopamine is inhibitory.

Meaning it slows things down.

It's the brake.

It's the brake.

It's the whoa, easy now signal.

It refines movement.

Acetylcholine, on the other hand, is excitatory.

It's the gas pedal.

Go, go, go.

Precisely.

It stimulates muscle contraction.

So you have this constant push and pull.

In a healthy brain, they're in perfect equilibrium.

The go signal is balanced by the slowdown signal, and the result is smooth, coordinated movement.

So what happens in Parkinson's disease?

The text is clear.

Parkinson's is a disease of dopamine deficiency.

The cells that make dopamine are dying.

So imagine the dopamine writer on the seesaw slowly getting smaller and smaller until he just falls off.

What happens to the acetylcholine side?

It slams down to the ground.

It becomes relatively dominant.

So it's not that the brain is suddenly making more acetylcholine.

Not at all.

The amount of acetylcholine is the same.

It's just that there's no dopamine left to counterbalance it.

So the excitatory side, the go side, is running wild, completely unchecked.

And that's the tremor.

Uncontrolled go signals.

That's the tremor.

That's the rigidity.

It's the result of unopposed excitation.

Your gas pedal is stuck to the floor and the brakes are gone.

That makes so much sense.

It's not just about a lack of one thing.

It's the unchecked power of the other thing.

Bingo.

And the text gets even more specific.

It takes us right to the anatomical location where this all goes down.

It mentions a structure called the substantia negra.

Which translates to the black substance.

It sounds like something from a fantasy novel.

It does, but it's actually a beautiful description of healthy biology.

The substantia negra is a small area in the midbrain.

In a healthy person, the cells there are darkly pigmented.

If you look at a cross section of a healthy brain, which is shown in figure 13 -2, you can see this distinct dark band.

And what's making it dark?

It's the melanin pigment inside the dopamine producing cells.

That darkness is the sign of a healthy, functioning dopamine factory.

So dark means healthy.

In this case, yes.

It means the factory is open for business.

But then, look at the other side of figure 13 -2.

It shows the brain of a patient with Parkinson's.

It's pale.

The black stripe is just gone.

It's faded.

The text calls it depigmentation.

The color fades because the cells have died.

The dopamine factory has literally shut down.

OK, so the factory is closed.

How does that affect the rest of the brain?

Well, a factory has to ship its product.

The dopamine made in the substantia negra is sent to another area called the basal ganglia, specifically the corpus striatum.

The pathway it travels on is called the negrostriatal tract.

Negrostriatal tract, so that's the highway.

That's the highway from the factory substantia negra to the warehouse basal ganglia.

When the factory closes, the highway is empty.

The warehouse receives no shipments of dopamine.

And as a result, the warehouse, the part of the brain that coordinates movement,

stops working correctly.

The seesaw tip's over.

OK, so that's Parkinson's disease.

Cells die.

Factory closes.

Seesaw tips.

But why do we in psychiatry care so deeply about this?

This is where the textbook sidebar Norm's Notes comes in.

Yeah, Norm's Notes are always gold.

And Norm points out this fascinating, almost perfectly inverse relationship.

It's one of those things that once you see it, the whole field of psychopharmacology just clicks into place.

Lay it on me.

Schizophrenia, specifically the positive symptoms like hallucinations,

delusions, disorganized thoughts, is associated with excess dopamine.

Too much dopamine.

Way too much.

The brain is flooded with it.

In this case, the seesaw is tipped the other way.

The dopamine side is slammed to the ground.

OK, wow.

So schizophrenia is high dopamine.

Parkinson's is low dopamine.

Correct.

They are, in a way, chemical opposites.

So how do we treat schizophrenia?

We give antipsychotic drugs.

And what do those first generation typical antipsychotics do?

They block dopamine receptors.

They're dopamine antagonists.

Exactly.

They are trying to lighten the load on the dopamine side of the seesaw to bring it back into balance.

I see exactly where this is going.

If you use a powerful drug to block dopamine.

You are artificially, chemically creating a state of low dopamine function.

You are inducing the exact same imbalance that happens organically in Parkinson's disease.

You cure the hallucinations, but you tip the seesaw so far back that the patient starts shaking and gets rigid.

That is the treatment dilemma in a nutshell.

You push down one symptom and another one pops up on the other side of the seesaw.

We're not dealing with cell death like in Parkinson's disease, but we're dealing with receptor blockade at the destination.

The end result for the patient, though, the shuffling, the tremors, it feels exactly the same.

The basal ganglia is being starved of dopamine one way or another.

Whether the factory is closed or the delivery trucks are all being blocked at the warehouse gate, the result is the same.

The warehouse is empty and it revolts.

Let's talk about that revolt.

This brings us to the next big section, defining extra pyramidal side effects.

We've tipped the seesaw.

Acetylcholine is running the show.

What does that actually look like minute to minute for a patient?

Because the text lists a whole spectrum of these EPSCs.

It's a spectrum that ranges from, let's say, deeply uncomfortable to acutely life threatening.

And as a nurse, you absolutely have to be able to spot all of them.

Let's start with the most common one, akathisia.

The text defines it as a subjective restlessness.

That sounds almost mild, like, oh, I'm a bit bored today.

It is anything but mild.

That clinical definition does it a terrible injustice.

The patient's experience is torture.

Patients describe it as an internal jitteriness, a motor restlessness that is impossible to ignore.

They feel like their legs are on fire or like they have to keep moving or their skin will crawl off.

So it's more than just restless leg syndrome.

Imagine restless leg syndrome in your entire body, magnified by 10, and it never, ever stops when you're awake.

The text notes that this is a major cause of nonadherence to medication.

I can see why.

Patients will literally say, I would rather hear the voices than feel this way.

It's also linked to agitation, aggression and even suicide.

It is that distressing.

You said it's often missed.

It's often misinterpreted because it's subjective, meaning only the patient can truly feel it.

We on the outside just see them pacing the hallway, unable to sit still.

What do we church?

Patient is agitated.

Exactly.

And what's the knee -jerk response to agitation in a psychiatric patient?

Give them more antipsychotics or a higher dose.

Which blocks more dopamine, which makes the akathisia worse.

It's horrifying, vicious cycle.

So the take home is if a patient says they feel jittery or can't sit still, believe them.

Don't just dismiss it as part of their psychosis.

Investigate.

That's a huge clinical problem.

OK, what's next on the list?

Akinesia and bradykinesia.

These are basically the opposites of akathisia.

Akinesia means without movement.

Bradykinesia, as we said, is slow movement.

You'll see the patient looking almost like a zombie.

They have profound weakness, fatigue, anoregia, which is just a total lack of energy.

This seems like it would be incredibly hard to distinguish from, say, severe depression or even the negative symptoms of schizophrenia itself, like abolition.

It is very, very difficult.

And it takes a sharp nurse to notice the difference.

Is the patient sitting in that chair all day because they're depressed and unmotivated?

Or is it because their dopamine is blocked so heavily that they physically feel like they're moving through molasses?

I would eat it to the difference.

One clue is that this often responds really well to the anticholinergic drugs we'll talk about later.

If you give a dose of cogentin and the patient suddenly perks up and starts engaging, you have your answer.

It wasn't just depression.

OK, so those are the chronic day to day miseries.

But then the text talks about the dystonias.

These sound much more dramatic and acute.

Dystonias are the emergencies.

These are involuntary sustained muscle spasms that result in abnormal, often painful postures.

The text says they usually appear early, often within the first three days of starting a new antipsychotic, especially a high potency one like Haldol.

Give us some examples.

What does a dystonia actually look like on the unit?

A very common one is torticollis.

That's a severe contraction of the neck muscles.

The patient's head is twisted to one side and they can't straighten it.

It's painful and very distressing.

OK, that sounds awful.

But the one that really, truly scares people, both the patients and the new nurses, is the oculodgeric crisis.

The name alone sounds like a sci -fi term.

It feels like a horror movie for the patient.

The muscles that control eye movement go into spasm and the eyes lock in an upward position.

The patient is staring at the ceiling and is physically unable to look down or forward.

I can't even imagine how terrifying that would be.

You're already being treated for psychosis.

You're maybe paranoid or delusional and suddenly your own body betrays you and you can't even control where your eyes are looking.

It's incredibly frightening and painful.

But the most dangerous dystonia, the one that is a true medical emergency, is laryngeal dystonia.

Laryngeal.

So that involves the throat, the larynx.

Yes, it's a pharyngeal constriction.

The muscles of the throat and larynx spasm and tighten up and this can directly compromise the patient's airway.

So they can't breathe.

Their breathing becomes labored.

They might have trouble speaking or swallowing.

This is potentially life -threatening.

If you see a patient on a new antipsychotic who is suddenly struggling to breathe, you need to act immediately.

And act, in this case, doesn't mean charting it and waiting for the doctor to call back in an hour.

It means getting the emergency drugs, the parenteral injectable anticholinergics, ready to go.

You cannot wait for a pill to digest when someone's airway is closing.

Okay, we also have drug -induced Parkinsonism, which is the cluster of the big four symptoms we already talked about.

And then there's something called Pisa syndrome.

Yeah, just like the Leaning Tower of Pisa, the patient's body is flexed to one side.

They're literally leaning over.

It can be acute or it can be tardive, meaning it comes on later.

The text notes that older adults are particularly vulnerable to this one and it's a huge fall risk.

Speaking of tardive, that brings us to the big one, the one that I think haunts psychiatric nursing more than any other side effect.

Tardive dyskinesia or TD.

This is the one we all wanna prevent.

Tardive, as you said, means late appearing.

This doesn't happen in the first week.

The textbook says this usually develops after about six months of continuous antipsychotic use, sometimes longer.

And the mechanism is different, right?

It's not just a simple dopamine blockade.

It's a cruel twist of biology.

We've been talking about blocking dopamine receptors for months or years.

The brain is an adaptive organ.

If you consistently block a receptor, the brain thinks, hey, I'm not getting any signal here.

I'm being starved.

So it tries to compensate.

How does it compensate?

It upregulates.

The dopamine receptors become hypersensitive.

They multiply and become desperate for any little bit of dopamine they can find.

So they become super reactive to any dopamine that does get through the blockade.

Exactly.

So now even a tiny amount of dopamine that slips past the antipsychotic causes a massive overblown response.

And this results in hypermovement,

dyskinesia, involuntary movements.

What do those movements look like?

The symptoms are classic and primarily affect the mouth and face, tongue writhing, tongue protrusion, what's often called a fly -catching motion of the tongue lips smacking, puckering, chewing motions, teeth grinding.

It's almost like the mouth has a mind of its own.

It does, constant purposeless movements.

And it's socially devastating.

Imagine trying to have a normal conversation or go on a job interview or eat a meal in a restaurant when your tongue is protruding rhythmically at every few seconds.

Can the patient control it at all?

The text makes two important points.

The symptoms stop during sleep.

And patients can sometimes suppress the movements willfully for a very short period of time if they concentrate hard, but as soon as their focus shifts, the movements come right back.

And the prognosis.

This is the scary part, right?

Can we fix it?

That is the tragedy of TD.

It is often irreversible.

Once those receptors have become hypersensitive, they may stay that way for life, even if you stop the medication that caused it.

That's absolutely terrifying.

It gets worse.

The text includes a crucial critical warning for any nursing student.

The anticholinergics, the drugs like cogentin that we use to treat all the other side effects we just discussed.

They usually make tardive dyskinesia worse.

Wait, what?

How?

The cure for the tremor makes the TD worse.

Yes, think about the seesaw again.

Anticholinergics work by lowering acetylcholine.

This tips the seesaw back towards a state of relative dopamine dominance.

Since TD is caused by hypersensitive dopamine receptors, anything that makes dopamine more dominant just fuels the fire.

It's like pouring gasoline on it.

So if you have a patient with TD, you are truly stuck between a rock and a hard place.

Which is why the text emphasizes that prevention is the only real strategy.

Catching it early, using the lowest effective dose of antipsychotics, and regular monitoring with tools like the Ames test, the abnormal involuntary movement scale.

Okay, there's one more side effect we have to cover before we move on to the treatments.

The text calls it rare, but potentially lethal.

Neuroleptic malignant syndrome, or NMS.

NMS is the absolute nightmare scenario.

It's rare, affecting less than 1 % of patients.

But the mortality rate, before we got good at recognizing and treating it, was as high as 20 to 30%.

It has dropped significantly due to better awareness, but if you miss it, your patient can die.

So what are the absolute key signs?

What distinguishes this from, say, a really bad dystonia?

The temperature.

The number one cardinal symptom is severe hyperthermia, and we are not talking about a low -grade fever of 100 .5.

We are talking 101, 103, and it can spike all the way up to 108 degrees Fahrenheit.

The body is literally cooking itself from the inside out.

My God, 108 degrees, that's brain damage territory.

Absolutely.

Along with that extreme fever, you see extreme muscle rigidity.

It's often called lead pipe rigidity.

The patient's limbs are completely stiff.

And third, you see autonomic dysfunction.

Meaning?

Their vital signs are all over the place, wildly fluctuating blood pressure, tachycardia, profuse sweating.

They are in a state of physiological chaos.

So high fever plus lead pipe rigidity in a patient on antipsychotics equals NMS until proven otherwise.

That is the equation you must remember.

Treatment is immediate.

Stop the offending antipsychotic immediately.

Start aggressive cooling measures, cooling blankets, ice packs in the armpits, and groin.

And then there are specific drugs like dantrolene, which is a muscle relaxant, and bromocryptin, which is a dopamine agonist.

You have to break the fever and the rigidity or they will go into rhabdomyolysis and multi -organ failure.

It is an incredibly heavy list of potential problems.

Acethesia, dystonia, TD, NMS.

It really drives home the point that you're not just handing out pills, you're managing a chemical weapon, in a way.

You absolutely are, and you have to know what to watch for.

Now, surely some people are more at risk than others.

Box 13 to one in the chapter gives us a populations at risk breakdown.

Who do we need to be watching with an eagle eye?

The text identifies four main groups that are at higher risk.

First, for reasons that aren't perfectly clear, women seem to be at a higher risk for developing EPSCs.

Okay, women, who's next?

Second, patients experiencing their first episode of schizophrenia.

That's interesting, why the first episode?

You'd think people on the drugs longer would be more at risk.

For TD, yes, but for the acute EPSCs, their brains are naive to the medication.

They haven't built up any tolerance or adaptation yet, so the shock to the dopamine system is much greater.

The response is more dramatic.

Makes sense, who's third?

Third is older adults.

Their systems are just more sensitive, and we'll talk more about the specific reasons why in a bit.

And fourth is patients with affective symptoms.

Meaning patients who also have mood disorders.

Exactly, patients who have major depression or bipolar disorder alongside their psychosis seem to be more vulnerable.

So if you have, say, a 68 -year -old woman admitted for her first psychotic break, and she has a history of depression.

She is a walk -and -talking bundle of red flags for EPSCs.

You watch her like a hawk.

All right, let's pivot.

We have thoroughly broken the system.

The seesaw is tilted, the patient is shaking, or their eyes are rolled back in their head.

How do we fix it?

We've teased it, but let's dive into part four of the chapter.

Pharmacologic treatment.

Okay, let's go right back to that seesaw.

This is the absolute key to understanding the meds.

The patient has schizophrenia, which we're treating as a high dopamine state.

We gave them an anti -psychotic, like heloperidol, to block that dopamine.

Now, the dopamine side of the seesaw is artificially low.

And because the dopamine side is low, the acetylcholine side is now relatively high, and that's causing the tremors and the rigidity.

Perfect.

So your first instinct, your logical thought, well, let's just give them some dopamine.

Let's level the seesaw by pushing the dopamine side back up.

That's what we do for regular Parkinson's patients.

We give them a drug called Lividopa, which is a dopamine precursor.

But we absolutely cannot do that here.

Why not?

Because if we add dopamine back into the system, we completely undo the effect of the anti -psychotic.

The psychosis comes roaring back.

The voices, the paranoia, we'd be right back at square one.

Exactly.

We would be fixing the side effect by recreating the original problem.

So we cannot touch the dopamine side of the seesaw.

It's off limits.

We have to work on the other side.

We have to work on the other side.

If we can't raise the low side, our only other option is to lower the high side.

We have to bring the acetylcholine down to match the new lower level of dopamine.

So the seesaw becomes level again, not because we raised dopamine, but because we lowered acetylcholine.

You were restoring the balance, but at a lower overall level of function.

It's a brilliant pharmacological workaround.

It's subtraction, not addition.

So the drugs that do this, the ones that block acetylcholine are called anticholinergics.

Okay, so let's meet the lineup.

The text lists three main players in this category.

First up is the MVP,

the go -to, the workhorse.

Benstropene, brand name, Cogentin.

I feel like every nurse, even student nurses, have heard of Cogentin.

It's everywhere on the internet.

It is the most frequently prescribed drug for EPSEs by far.

It's used for all the Parkinsonian -like disorders, the dystonias, the rigidity, the tremors.

And the great thing about Cogentin is its versatility in how you can give it.

It comes in different forms.

Right, it comes in oral tablets, Piotone.

But crucially, it also comes in IM, intramuscular, and 5E, intravenous forms.

And why does the form matter so much?

Speed, it's all about speed.

If a patient has a mild, ongoing tremor, you give them a pill every day.

It works great.

But if that patient is in an acute oculodgeric crisis with their eyes locked back, or a laryngeal dystonia where their airway is tightening.

You don't have time for a pill to digest.

You need that drug in their bloodstream now.

That's when you use the IM or IV route for rapid relief.

Got it, okay, who is number two in the lineup?

Number two is Diffinhydramine.

And you absolutely know it by its brand name, Benadryl.

The allergy medication, the pink pill.

The very same.

Benadryl is a potent antihistamine, but it also has very strong anticholinergic properties.

It's quite effective for EPSEs, particularly acute dystonias.

But it has one very famous side effect that anyone who's taken it for hay fever knows all too well.

It knocks you out cold.

Sedation.

Major sedation.

It makes you incredibly sleepy.

Now sometimes that can be a benefit if the patient is agitated and needs to calm down, but often it's a drawback.

The text has a fascinating little comparison in table 13 .3 that shows the potency difference.

Yeah, I saw that.

It says 50 milligrams of Benadryl has the equivalent anticholinergic effect of just one milligram of Cogentin.

Think about that.

That tells you just how powerful Cogentin is.

You need 50 times the mass of Benadryl to get the same anticholinergic punch as one tiny crumb of Cogentin.

Wow.

Okay, and the third drug on the list.

The third one is Trihexafenadol, brand name Artane.

Artane.

That sounds like an older drug.

It is.

It's an older drug, and it's used less often now for a very specific reason.

It has no parenteral form, no injections, it's pills only.

Ah, so you would never use Artane for an emergency.

Never.

You'd never use it for an acute dystonic reaction because you simply can't get it into the patient's system fast enough.

It's reserved for ongoing prophylactic management of milder symptoms.

That's a key clinical pearl right there.

If the patient is in an acute crisis, you're leaving the Artane on the shelf.

You're grabbing the injectable Cogentin or Benadryl.

100%.

Now the text gives us a table, table 13 to four, with some standard dosages.

It's not about memorizing, but getting a feel for the ranges.

For Cogentin, it's usually one to four milligram, maybe once or twice a day for maintenance.

For an acute dystonia.

For an acute crisis, it's a stat order, usually one to two milligram IM or IV.

You can repeat it in 15, 30 minutes if you don't get a response.

Okay, so we've solved the movement problem.

We gave the Cogentin IM, the patient's neck relaxed, their eyes came down, the seesaw is balanced.

We're heroes.

Right.

But biology is never that kind.

There's no such thing as a free lunch in pharmacology.

Never, ever.

By giving an anticholinergic, we are solving one very serious problem, but we are absolutely creating a whole new set of potential side effects.

We are deliberately blocking acetylcholine.

Acetylcholine does a lot of other really important work in the body.

Both in the brain, the CNS, and in the peripheral nervous system, the PNS.

Right, and you'll see side effects in both.

Let's talk about the brain first.

What are the CNS effects of blocking acetylcholine?

Acetylcholine is a crucial neurotransmitter for memory, learning, and concentration.

It's the cognitive neurotransmitter.

It's the one that's deficient in Alzheimer's disease.

So if you block it - They get brain fog, you make it harder to think.

Exactly, you can get confusion, cognitive impoverishment, agitation, dizziness, and the text makes a really poignant observation here.

Our patients, the ones with schizophrenia,

often already suffer from significant cognitive deficits.

It's a core part of the disease.

So by treating the side effects of their antipsychotic meds, we might be making their cognitive symptoms worse.

That sounds harsh, but - We might be blunting their cognitive abilities, yes.

It's an incredibly difficult trade -off.

Do you want the patient to be able to walk without shuffling or do you want them to be able to concentrate on reading a book?

Sometimes you have to find a middle ground because you can't have perfection.

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

Constantly balancing the lesser of two evils.

Okay, now let's talk about the body.

The PNS effects.

The text calls these the antiparasympathetic effects.

And that's the best way to remember them.

Think about your autonomic nervous system.

Your parasympathetic system is your rest and digest system.

It's what makes you salivate.

It keeps your gut moving.

It helps you urinate.

It keeps your heart rate slow and steady.

So an anticholinergic drug turns that entire system off.

It blocks it.

So everything that should be wet becomes dry and everything that should be slow becomes fast.

The text is a great breakdown using the cranial nerves in table 13 to six, which is perfect for students studying their anatomy.

Let's run through the big ones.

Cranial nerve three.

The oculomotor nerve.

This nerve controls the muscles that constrict your pupil.

If you block acetylchole's effect on it, you get mediasis.

The pupil dilates and stays wide open.

Which would cause blurred vision.

Blurred vision, especially up close because you can't accommodate.

And photophobia, extreme light sensitivity, everything looks painfully bright.

Okay, what about cranial nerves seventh and IX?

The facial and glossopharyngeal.

Those control your salivary glands.

Block them and you get xerostomia severe dry mouth.

And we are not talking about just feeling a little thirsty.

We're talking about a mouth so dry it's like cotton, which makes it hard to speak or swallow food and it massively increases the risk of cavity.

And then the big one, cranial nerve X.

The vagus nerve.

The vagus nerve is the superhighway of the parasympathetic system.

One of its main jobs is to act as the brake pedal for the heart.

It keeps your resting heart rate nice and slow, maybe 60 or 70 beats per minute.

If you block the vagus nerve with an anticholinergic.

You cut the brake lines.

And the heart ticks off, tachycardia.

The heart rate jumps up.

The text warns that this is a serious concern, especially for older patients or anyone with a pre -extinct cardiac condition.

The text provides a really helpful table.

Table 13 to five.

That's all about nursing interventions for these specific symptoms.

Let's do a rapid fire round for our listeners.

I'll give you the common anticholinergic side effect.

You give me the key nursing intervention.

Let's do it, hit me.

Dry mouth.

Sugarless candy or gum to stimulate whatever saliva is left.

Frequent sips of water or mouth rinses.

And absolutely crucial.

Tell them not to use sugary candy or they'll rot their teeth out since they have no protective saliva.

Nasal congestion.

An OTC saline nasal spray can help, but they should check with their provider before using any decongestants as those can have their own side effects.

Urinary retention.

This is a big one, especially for men.

A huge one.

Monitor the intake and output.

If your patient hasn't peed in eight hours, that's a red flag.

You need to assess them maybe with a bladder scanner.

It happens because the blower muscle loses its squeeze tone.

They might need to be catheterized to drain the bladder.

Word vision.

Reassurance is key.

Tell them it's the medication, they are not going blind.

Advise them that tolerance often develops over a few weeks.

In the meantime, wear sunglasses for the photophobia and be very cautious about driving.

Constipation.

Remember, we slowed down the gut.

So you need to get it moving again.

High fiber diet, encourage fluid intake.

The book recommends 2 ,500 to 3 ,000 millilits a day and have a low threshold to use stool softeners or laxatives per the doctor's orders.

And the last one, decrease sweating.

This one is sneaky dangerous, especially in the summer.

The body can't cool itself properly without sweat.

This puts them at a high risk for overheating and heat stroke.

The interventions are environmental, keep them cool, use sponge baths, and teach them to limit strenuous activity in hot weather.

Now, box 13 to two in the chapter lists some very serious risks.

We talked about how these drugs can induce psychosis, which is the ultimate irony.

But it also mentions they can be lethal in overdoses.

Oh yes, anticholinergic toxicity is a full -blown medical emergency.

And there's that classic rhyme that every med student and nursing student learns to recognize the symptoms.

You gotta know this one.

Hot as a hair, dry as a bone, mad as a hatter, red as a beet.

Let's break that down for them.

Hot as a hair.

Hyperparexia.

They have a high fever because they can't sweat.

Dry as a bone.

No sweat, no saliva, no tears.

Their mucus membranes are like sandpaper.

Mad as a hatter.

This is the CNS toxicity.

They are confused, delirious, agitated, and can have vivid hallucinations.

And red as a beet.

They have flushed skin.

It's because the blood vessels in the skin dilate as the body desperately tries to dump heat that it can't get rid of through sweating.

So if you see that combination of symptoms.

You call a rapid response.

The patient is in anticholinergic poisoning.

It can progress to seizures, coma, and death if not treated.

We've mentioned older adults a few times, but box 13 to three in the chapter really focuses on them.

Why are they so exquisitely sensitive to these drugs?

It comes down to three main things according to the text.

One, slower metabolism.

Their liver doesn't break down the drug as fast so it hangs around longer and builds up to higher levels.

Okay, that makes sense.

Two, slower elimination.

Their kidneys aren't filtering as efficiently as a younger person's.

And three, and this is the most important one, their brains often already have a baseline deficit in cholinergic transmission.

What do you mean?

As we age, we naturally lose some acetylcholine function.

It's part of the reason why memory can fade.

So they are already starting with a tank that's only half full.

If you give them a drug that blocks what little acetylcholine they have left.

You push them right off a cognitive cliff.

Instantly.

You can see profound confusion and delirium from just one small dose of cogentin in a vulnerable older adult.

The text also specifically warns about benign prostatic enlargement or BPH.

The prostate, how does that connect?

Many older men have an enlarged prostate which already makes it difficult for them to urinate.

If you then give them an anti -cholinergic which relaxes the bladder muscle and makes it harder to squeeze, you can cause complete urinary retention.

He won't be able to pee at all which is another medical emergency.

Another great tip, always check the prostate history before you push that first dose of cogentin.

What about drug interactions?

What should patients on these meds avoid?

The big one is not to double dip.

They must avoid over -the -counter cough and cold medicines because many of them like NyQuil or even Benadryl itself contain antihistamines with strong anti -cholinergic properties.

So they'd be getting a double dose.

A double dose which can lead to toxicity.

They should also avoid alcohol as it enhances the sedative effects.

And the text notes that antacids can decrease the absorption of anti -cholinergics so they shouldn't be taken at the same time.

And what's the most important piece of patient teaching?

Do not stop taking it abruptly.

These drugs need to be tapered over about a week.

If you stop cold turkey, you can get a nasty cholinergic rebound syndrome.

Your body suddenly has all this unblocked acetylcholine leading to vomiting, sweating and nightmares.

We are getting near the end of the chapter now.

Part seven covers prevention and other treatments.

Are anti -cholinergics the only game in town?

No, there are a few other options and they work through different mechanisms.

The text mentions amantadine, brand name Symmetrol.

This one is interesting because it's actually a weak dopamine agonist.

It encourages the release of what little dopamine is available.

But wait, I thought we couldn't add dopamine back in.

Amantadine is gentle enough that it usually doesn't trigger psychosis.

It can provide just enough of a dopamine boost to help with the movement symptoms without undoing the anti -psychotic effect.

But it's a delicate line to walk.

What else?

Propranol, brand name Inderol.

This is a beta blocker.

It has nothing to do with dopamine or acetylcholine.

It works on the adrenaline system and it is fantastic for treating akathisia, that awful inner restlessness.

And benzodiazepines.

A benzo like Valium or Ativan can sometimes help relax the muscles during an acute dystonia, but they're addictive and sedating, so they're used with caution.

The text also mentions a couple of vitamins E and B6.

Yeah, there's some empirical support, though not definitive, that high doses of vitamin E and B6 might help diminish the severity of tardive dyskinesia.

It's not a cure by any means, but given that vitamins are low risk, it's often worth a shot.

But the best treatment of all is prevention, always.

The chapter lays out a clear strategy.

First, identify the high -risk groups we talked about.

Second, get a baseline assessment before you start the anti -psychotic.

Use the AIMS test.

Use the AIMS test at baseline and then regularly.

Third, when possible, choose lower -risk anti -psychotics.

The newer, atypical agents like clozapine or quitapine generally have a much lower risk of causing EPSCs than the old typicals, like haloperidol.

And finally, if EPSCs do develop, the first step should always be to consider lowering the dose or switching the drug before you just add another pill like cogentin on top.

Let's bring all of this together now.

The text ends with a powerful case study.

I wanna walk through this with you because it really paints a perfect picture of what a nurse actually does in these situations.

Okay, let's do it.

Set the scene for me.

We have a 25 -year -old woman.

She was admitted for an acute psychotic episode and was started on haloperidol, Haldol.

A few days later, she's walking down the hall and starts telling the nurse she feels slow.

Okay, so that's the bradykinesia setting in.

Her dopamine is being effectively blocked.

Right, she sits down in the day room.

Then suddenly, crisis.

Her neck muscles contract violently, pulling her head all the way back.

At the same time, her eyes roll upward and lock on the ceiling.

Torticollis and an oculodgeric crisis happening together and she is now terrified.

She is acutely psychotic and her body is doing something bizarre and uncontrollable.

She's likely thinking, am I possessed?

Is this part of the illness?

She doesn't understand it's a side effect.

And then her breathing becomes labored.

That's the laryngeal dystonia kicking in.

The muscles in her neck and throat are spasming, compressing her airway.

This is a full -blown emergency.

You are the nurse who walks in and sees this.

What do you do?

You don't panic, you don't call a consult and wait.

You immediately check the PRN medication orders and you see an order for benstropine, cogentin, two milligram IM for acute dystonia.

You grab the vial, draw it up into a syringe and you administer it, probably into the deltoid or gluteal muscle.

Okay, in the case study, the nurse gives the shot.

But 15 minutes go by.

There's no change.

She's still locked up, struggling.

And that can happen.

The first dose isn't always enough.

You check the order again and it likely says may repeat in 15, 30 minutes.

The nurse in the case study gives a second two milligram dose.

And what's the result?

The tech says that within five minutes of that second dose, the muscles begin to relax, her eyes come down, she can move her neck again, she can breathe easily.

She is, for all intents and purposes, back to her normal.

That is incredibly dramatic.

To go from I can't breathe and I can't see to fine in the span of 20 minutes, all because the nurse recognized the symptoms and knew what drug to give.

That is the power and the responsibility of pharmacology and psychiatric nursing.

And it highlights why you need to do patient teaching before it happens.

Tell your patients on Haldol, hey, there's a rare chance your muscles might get stiff.

If that happens, tell me immediately.

We have a shot that fixes it almost instantly.

That education removes so much of the fear.

We have covered a massive amount of ground today.

The biology of the seesaw, the horror of the symptoms, the logic of the drugs and the critical nursing care.

Let's finish by doing a quick fire recap of the study note summary from the end of the chapter.

Let's distill it down to the absolute essentials.

One, Parkinson's disease is a degeneration of the substantia nigra cells.

The cause is unknown.

Two, EPSCs or Parkinsonism are caused by a receptor blockade from antipsychotic drugs.

The cause is us.

Three, normal movement requires a balance on the seesaw.

Dopamine, which is inhibitory, versus acetylcholine, which is excitatory.

Four, the four cardinal symptoms of PD are tremor, bradykinesia, rigidity, and postural instability.

Five,

PD treatment involves trying to increase dopamine, usually with L -Dopa.

Six, EPSC treatment involves blocking acetylcholine with drugs like cogentin because we cannot increase dopamine in our patients with psychosis.

Seven, the major drugs we use are the anticholinergics, benzotropine, diphenhydramine, and trihexafanadol.

Eight.

And finally, older adults are extremely sensitive.

Watch them closely for confusion and urinary retention.

That's the cheat sheet.

If you know those eight points, you have a solid grasp of this chapter.

But if you take only one single thing away from this entire deep dive, remember the seesaw.

It's all about the balance.

And a final thought for our listeners to take with them.

These drugs, the anticholinergics, they manage side effects.

But your real goal as a nurse is prevention and early detection.

You are the one at the bedside.

You're the one watching the patient walk down the hall every hour.

You spot the subtle tremor before it becomes a fall.

You spot the restless pacing and identify it as akathisia before it becomes a suicide attempt.

You are the early warning system.

Absolutely.

The drugs are just tools in the toolbox, your observation, your assessment, your clinical judgment.

That's the safety net.

Thank you so much for trusting the Last Minute Lecture Team with your study time.

We know this stuff is dense, but you are doing the hard work and that matters more than you know.

Good luck on your exams.

You got this.

You see you in the next deep dive.