Chapter 20: Parkinson & Alzheimer Disease Drug Therapy

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Welcome back to the Deep Dive.

Today, uh, feels a little different.

It does.

Usually we're bouncing around between articles, broad concepts, but today we have a very, very specific mission.

We do.

We're on a mission.

We are cracking open chapter 20 of pharmacology,

a patient -centered nursing process approach.

And honestly, just looking at this chapter, it feels like we're walking straight into the neurology ICU.

It absolutely does feel that way.

We are definitely dealing with the heavy hitters of neuropharmacology today.

We're not talking about, you know, mild ailments.

We are looking at Parkinson disease and Alzheimer disease.

Two giants.

I mean, one strips away your ability to move and the other, it strips away your ability to think.

Yeah.

Your very self.

That is the tragedy of it.

And it's also the, uh, the pharmacological challenge.

These are progressive degenerative conditions.

We don't have cures.

We have management strategies.

And for the nursing students or the clinicians listening, understanding the drugs just isn't enough.

It's not.

You have to understand the wiring diagram of the brain to even begin to know why we're throwing these specific chemicals at it.

That's the goal for this hour, right?

We're going to decode this dense textbook material.

We're going to take those incredibly complex tables about receptor agonists and enzyme inhibitors and turn them into a clear linear narrative.

Because if you just memorize Lodopa, you'll forget it by the board exam.

But if you understand the why, the mechanics of the blood brain barrier and the, I don't know, the neurotransmitter wars, you'll never forget it.

And more importantly, you'll know what to look for when you're standing at the bedside.

Yes.

Because the side effects of these drugs can be just as debilitating as the diseases themselves if we aren't incredibly careful.

Okay.

So let's start with the movement disorder, Parkinson disease or PD.

Let's do it.

The text defines it as a chronic progressive neurologic disorder affecting the extrapyramidal motor tract.

Now I've always found that term extrapyramidal to be a bit of a conversation stopper.

It sounds intimidating, doesn't it?

It does.

What are we actually talking about here?

It really does sound intimidating, but think of it like this.

You have your main motor tract, that's the pyramidal tract, and it controls your voluntary movement.

Okay.

Like I want to pick up this pen.

That's the direct order from headquarters.

Got it.

The extrapyramidal tract is the autopilot.

It's the background system that handles your posture, your balance, the smoothness of that movement.

So it's what keeps me from like falling out of my chair while I reach for the pen.

Exactly.

And it ensures your hand doesn't shake while you're doing it.

It's all the automatic stuff we take for granted.

So when that system goes offline, the autopilot just crashes.

It crashes hard.

Exactly.

You lose that background stability, that smoothness.

And that's what gives us the syndrome of Parkinsonism.

It's not just one thing, it's a whole cluster of symptoms.

Right.

The text lists three major ones that essentially define the condition.

Rigidity, breadykinesia, and tremors.

Let's break those down because they look very, very specific in a patient.

Rigidity isn't just stiffness like, you know, after a tough day at the gym.

No, not at all.

This is an abnormal increased muscle tone.

It's a constant resistance.

The text points out something really fascinating.

The rigidity often gets worse when the patient tries to move.

So the harder they try, the stiffer they get.

Can you imagine how frustrating that is?

It's like fighting your own body with every single movement.

Unbelievable.

Then we have breadykinesia.

Brady meaning slow, kinesia meaning movement.

But it's more than just being slow, isn't it?

It's so much more.

It's the difficulty in initiating the movement.

Imagine you want to stand up from a chair.

Your brain sends the signal, but the body just lags.

There's this profound disconnect.

And this is often the most disabling symptom of all because it affects absolutely everything.

Walking, eating, dressing, talking.

And that leads right into the gait disturbances.

The text describes this very distinctive walk.

The shuffle.

Yeah.

If you watch a healthy person walk, they have this natural arm swing.

Left leg forward, right arm forward.

It's a counterbalance.

In Parkinson's, that arm swing just, it vanishes.

The arms just hang there limp.

The patient takes these short shuffling steps and they're often leaning forward.

Which of course leads to the tremors.

This is usually the first thing people notice, the most obvious sign.

It is.

It's the pill rolling tremor.

And it looks exactly like it sounds.

The thumb and forefinger moving back and forth as if they're rolling a tiny invisible pill.

But the key here, and this is a major exam point and a huge clinical distinction, is that these are resting tremors.

Meaning they happen when the patient isn't doing anything.

When their hands are just in their lap.

Precisely.

If they go to reach for a cup of coffee, the tremor might actually stop or get better.

It's when their hands are at rest that the shaking starts.

It can affect the head and the neck too, but the hands are just classic.

The text also paints a really vivid and kind of sad picture of the patient's face.

It calls it masked facies.

It's heartbreaking to see.

The facial muscles become rigid, just like the rest of the body.

The patient loses the ability to smile or frown or show surprise easily.

They just stare.

Wow.

And it can make family members feel like the person they love is disengaged or emotionless.

But inside, they're feeling everything.

They just can't show it on their face anymore.

Plus that posture you mentioned.

Chest forward, head forward, knees bent.

They look like they are constantly on the verge of falling forward.

Which they are.

The fall risk is absolutely massive in this population.

It's a constant worry.

Okay, so that's the what.

A pretty clear picture of the physical decline.

Now we need the why.

This is where the pharmacology really starts to matter.

We have to go deep into the brain to the substantia negra.

What is this?

This chemical civil war that's happening in a Parkinson's brain.

It's a battle.

A battle between two key neurotransmitters in a part of the brain called the striatum.

You've got dopamine and you've got acetylcholine or acanchu.

Okay.

In a healthy brain, these two are in this beautiful delicate balance.

Dopamine is inhibitory.

It basically tells the neurons to chill out to control their firing.

Acetylcholine is excitatory.

It's the one telling them to go, go, go.

That's interesting.

I think a lot of people get that backward.

We usually hear about dopamine as the reward chemical, the do it again chemical.

But here in the motor track, it's the brake pedal.

In the specific context, yes, that's a perfect analogy.

Dopamine inhibits the release of another chemical called GAVA.

It keeps the motor neurons from overfiring.

Acetylcholine, on the other hand, stimulates them.

Okay.

So for smooth controlled movement, you need the gas pedal, ACHA, and the brake pedal, dopamine, working together in harmony.

But in Parkinson's, the substantia nigra, which is the factory that makes the dopamine,

it starts dying off.

Right.

The dopaminergic neurons, they degenerate.

So you're losing your brakes.

But the gas pedal, the acetylcholine, is still floored.

It's going full throttle.

And that's what leads to the unchecked cholinergic dominance.

You've got it.

You have way too much go signal and not enough stop signal.

So the rigidity and the tremors are essentially the muscles being constantly overstimulated because there's no dopamine there to say, whoa, stop, calm down.

The excessive acetylcholine stimulates the release of GAVA, and all that runaway excitation causes the symptomatic chaos we see.

So logically, our pharmacological strategies, it sounds simple on paper.

Either we find a way to boot the dopamine or we find a way to block the acetylcholine.

That is the entire game plan in a nutshell.

Okay.

But before we even start prescribing, we have to talk about the imposter.

The text has a really important section on pseudo -Parkinsonism.

This is huge for nursing assessment, isn't it?

Just because it walks like a duck and quacks like a duck.

Doesn't mean it's Parkinson's disease.

Idiopathic PD is the disease we just described.

The cause is unknown.

It's a slow degeneration over time.

Pseudo -Parkinsonism is something we did to the patient.

It's an adverse reaction to a drug.

And the text points the finger squarely at neuroleptics, antipsychotics, and other dopamine antagonists.

Well, think about it.

It makes perfect sense.

If you have a patient with, say, schizophrenia,

you might give them an antipsychotic to block dopamine receptors because too much dopamine in other parts of the brain can cause psychosis.

But the drug doesn't know which part of the brain it's in.

It's not that smart.

It blocks dopamine receptors in the motor track, too.

So you artificially create a dopamine deficiency, and boom, they start shuffling and shaking and looking just like a Parkinson's patient.

And we call these extra pyramidal symptoms, or EPS.

You see acute dystonia, which is these painful muscle spasms, akathisia, which is that horrible,

restless, crawling out of your skin feeling, and tardive dyskinesia, the repetitive face and mouth movements.

And the big scary one, neuroleptic malignant syndrome.

That's the emergency.

The true drop everything and call the doctor moment.

High fever, extreme rigidity, altered mental status, autonomic instability.

So if you see a patient on something like haloperidol, who suddenly gets rigid and spikes a fever, you don't treat them for Parkinson's.

You stop the antipsychotic immediately and you get them to the ICU.

That's a medical emergency.

So clinical judgment point number one, always, always check the med list.

If they are on haloperidol or even something like metoclopramide for nausea,

it might not be Parkinson's.

Exactly.

Always look for the reversible causes first.

All right.

Let's assume it is idiopathic Parkinson's.

Before we open the medicine cabinet, the text discusses non -pharmacologic measures.

It lists things like patient teaching, exercise, and nutrition.

Exercise seems particularly emphasized.

It's absolutely crucial.

You can't reverse the degeneration of the neurons, but you can fight the effects on the muscles.

Okay.

A good therapeutic exercise program keeps the joints mobile, improves flexibility and balance.

It is strictly use it or lose it.

If a Parkinson's patient stops moving, they will solidify.

And nutrition.

I know constipation is a recurring theme in this chapter.

It is the bane of these patients'

existence.

The disease itself slows down gut motility.

And as we'll see, the drugs we're about to discuss slow it down even more.

A double whammy.

It is.

They need fiber and fluids like it's their job.

It has to be a conscious part of their daily routine.

Now, there is a specific sidebar in the text about cannabis.

We can't ignore this because patients will ask about it.

They will.

Hey, I saw a video on YouTube where a guy smokes marijuana and his tremor stop.

What does the text actually say about this?

It acknowledges the interest.

Absolutely.

But it's very, very cautious.

It says that studies haven't conclusively proven a direct benefit for the core motor symptoms of PD.

But the real warning, the big red flag in the text, is about the cognitive side.

Executive function.

Right.

Cannabis is known to affect executive function.

Things like planning, decision making, risk assessment.

Well, Parkinson's disease also impairs executive function as it progresses.

So you're compounding the problem.

You're potentially compounding a cognitive deficit.

The text basically says,

proceed with extreme caution because you might make the thinking part of the disease worse.

Even if the tremors seem to settle down for a bit, it's a risky trade off.

That brings us to the drug strategy.

We have five categories outlined in the text.

Give us the roadmap.

What are our options?

Okay.

We're always chasing that balance.

So our strategies are, one, anticholinergics.

We block the acetylcholine, the gas pedal.

Got it.

Two, dopaminergics.

We try to replace the dopamine, basically refilling the brake fluid.

Three, dopamine agonists.

These are drugs that mimic dopamine.

They trick the receptors.

The impersonators.

The impersonators, exactly.

Four, MAOB inhibitors.

These stop one of the enzymes that eats dopamine.

And five,

COMT inhibitors, which stop the other enzyme that eats dopamine.

Okay.

A multi -pronged attack.

Let's start with the first group.

Anticholinergics.

Historically, these were the first line of defense, weren't they?

They were way back before we knew how to replace dopamine.

All we could do is try to block acetylcholine.

They are parasympatholitics.

They inhibit the release of ash.

And by reducing that cholinergic activity, they help with the rigidity and the tremors?

Yes.

They're actually quite good for tremors.

The text notes, though, that they have minimal effect on bradyacinegia, that slow movement.

So if the patient's main problem is that they can't get out of a chair, these aren't going to help much.

The specific drugs listed are benztropine and trihexafenadol.

Benztropine is one I see a lot in the hospital setting.

You do.

And you see it used mostly for that drug -induced Parkinsonism we just talked about.

If a patient gets stiff and trembly from an antipsychotic, we give them benztropine to loosen them up.

It's very effective for that.

But the side effects.

Oh, boy.

We have to talk about the anticellular DG effects.

This is a classic nursing mnemonic.

It's one you have to know.

Cholinergics make you wet.

They cause salivation, lacrimation, urination, defecation.

So anticholinergics dry you out.

Completely.

Completely.

Table 20 .2 in the text is just a laundry list of dry xerostomia, which is severe dry mouth,

urinary retention,

constipation, blurred vision, dry eyes.

And the urinary retention is so dangerous.

If a patient, say an older man, has an enlarged prostate, this can shut his bladder down completely.

It can cause complete obstruction.

It's a medical emergency.

There are also some hard contraindications.

The text is very clear on this.

Glaucoma is the big one.

Specifically, closed -angle glaucoma.

These drugs can increase intraocular pressure.

You can literally blind a patient if you aren't careful.

Also, myasthenia gravis, because that's a disease of muscle weakness.

And these drugs will just make it worse.

And there is a very specific bolded warning about the elderly population.

The text advises avoiding anticholinergics in older adults.

Which is such a cruel irony, isn't it?

Because most Parkinson's patients are older.

Right.

But anticholinergics in the elderly are notorious for causing confusion,

memory loss, and hallucinations.

It's often called anticholinergic toxicity, or the old saying, mad as a hatter.

So if a patient already has some underlying dementia, benztropine could push them right off a cognitive cliff.

Absolutely.

You could induce a delirium that's worse than the symptom you were trying to treat.

So use with extreme caution.

Okay.

Let's move to the main event.

The gold standard.

Dopaminergics.

Levodopa and Carbidopa.

This is it.

This is the revolutionary treatment.

Levodopa was introduced back in 1961, and it changed everything.

But the story of why we use levodopa and not just plain dopamine is one of the most interesting and elegant parts of pharmacology.

The blood -brain barrier problem?

It's all about the BBB.

The brain is a fortress.

It has this incredible wall of the blood -brain barrier that keeps toxins and random chemicals from just wandering in.

And dopamine, the chemical itself, cannot cross that wall.

It's too big.

It doesn't have the right key.

It's locked out.

So you can inject dopamine into a patient's veins all day long, but absolutely none of it will get to the substantia nigra where it's needed.

None of it.

It will just mess up their heart and their gut and make them vomit.

But levodopa, levodopa has a special pass.

It can cross the barrier.

And once it's safely inside the brain, an enzyme called dopa decarboxylase converts it into dopamine.

It's a Trojan horse.

It goes in, disguises levodopa, and then boom, it transforms into the medicine we actually need once it's inside the city walls.

That's the perfect analogy for it.

But there was a massive, massive problem with the original levodopa pills.

What was that?

That enzyme, dopa decarboxylase, it isn't just in the brain.

It's everywhere.

It's in your stomach, your intestines, your blood.

Oh, no.

So you take the pill and the enzyme attacks it immediately in the gut.

Immediately.

About 99 % of the levodopa was getting converted to dopamine in the periphery, in the body, before it ever had a chance to reach the brain.

That's a disaster.

It is, for two reasons.

First, the brain gets almost nothing, so the therapeutic effect was minimal.

Second, you now have these massive amounts of dopamine floating around in your blood.

Which causes?

Severe nausea, vomiting, palpitations, wild swings in blood pressure.

Patients were absolutely miserable on it.

Enter carbidopa.

The text calls this the solution, and it's brilliant.

Figure 20 .1 in the book shows this beautifully.

Carbidopa is a bodyguard.

Its only job is to inhibit that enzyme, dopa decarboxylase.

But, and this is the genius part, carbidopa cannot cross the blood -brain barrier.

That is so clever.

Carbidopa travels in the blood, protecting the levodopa from being eaten by the enzyme.

It's like an armed escort to the gates of the brain.

That's it.

And then levodopa crosses into the brain, leaving its bodyguard, carbidopa, behind.

Once inside the brain, there is no carbidopa to stop the conversion, so the levodopa is finally free to turn into dopamine where we need it.

It's one of the most elegant solutions in all of medicine.

The text says the ratio is usually one part carbidopa to ten parts levodopa.

And because of this combo, we can give much smaller doses of levodopa and get way, way better results with far fewer systemic side effects.

It completely changed the game.

Let's talk about the forms.

We have oral pills,

obviously, immediate and extended release.

But the text mentions levodopa inhalation.

Why would we need to inhale it?

This is for the off periods.

We really need to define on and off because this concept dominates the life of a Parkinson's patient.

Okay.

On is when the meds are working.

You can move.

You feel relatively normal.

Off is when the meds wear off before the next dose is due, or sometimes they just stop working randomly.

The patient freezes.

They just get stuck.

Literally stuck.

Can't move a muscle.

The inhalation powder is a rescue medication for those moments.

It bypasses the digestive system entirely.

It goes from the lungs to the blood to the brain very, very fast.

A lifesaver.

Okay.

Now, despite the carbidopa bodyguard, we still have adverse effects.

The prototype drug chart lists GI issues.

Nausea and vomiting are still very common.

They are.

Because some dopamine is still being produced in the gut, and even the dopamine in the brain can trigger the brain stem's vomiting center.

Dopamine stimulates the CTZ, the carrier receptor, trigger zone.

That's the vomit button.

The text suggests taking it with food to help with the nausea.

But there is a very, very specific catch about what kind of food.

Protein.

This is a vital, non -negotiable patient teaching point.

Okay.

Levodopa competes with amino acids from protein for absorption in the intestine and for transport across the blood -brain barrier.

If you eat a big steak dinner and take your levodopa, the protein will win that fight.

The drug won't work.

Wow.

We'll come back to that in the nursing process, but that is a huge deal.

What about cardiovascular effects?

Orthostatic hypotension is a big one.

The blood pressure plummets when they stand up.

You combine that with the shuffling gait and the balance problems.

It's a recipe for hip fractures.

And the neurologic side effects.

I find this so paradoxical.

The drug that treats movement disorders can actually cause other movement disorders.

Dyskinesia.

Yes.

If the dopamine levels in the brain peak too high, the patient starts having these involuntary, jerky, writhing, dance -like movements.

So it's a tightrope walk.

The tightest of tightropes.

Too little drug.

You're frozen and rigid.

That's Parkinsonism.

Too much drug.

You're flailing and writhing.

That's dyskinesia.

And finding that sweet spot in the middle gets harder and harder the longer a patient has the disease.

There are also psychiatric effects.

The text mentions hallucinations, nightmares,

and these impulse control symptoms.

This is the one that can destroy families.

Dopamine is the molecule of desire, of motivation, of reward.

When we flood the brain with it, we can sometimes trigger these intense compulsive behaviors.

Like what?

Pathological gambling, hypersexuality, compulsive shopping, binge eating.

You hear these stories of 80 -year -old grandmothers who have never gambled in their life, suddenly blowing their life savings online.

And it's the drug.

It is not a character flaw.

It's a neurochemical side effect.

Nurses have to be brave enough to ask about this and warn families that it can happen.

One last physical change that might scare the living daylights out of a patient if they aren't warned about it.

The urine and sweat discoloration.

It can turn the urine, sweat, even saliva, a reddish, brown, or black color.

Imagine waking up and your sweat has stained your bedsheets black.

You'd think you were dying.

I would panic.

Everyone would.

It's chemically harmless, just a metabolite of the drug, but you have to warn them so they don't panic.

And contraindications.

What are the absolute no -goes?

Glaucoma again.

Yes.

And suspicious skin lesions.

For some reason, levodopa can activate malignant melanoma, so a thorough skin check is part of the initial assessment.

And absolutely no MAOI therapy concurrently.

That is a hypertensive crisis.

Just waiting to happen.

Okay.

Moving on to section five.

Dopamine agonists.

How is an agonist different from what we just talked about?

Levodopa becomes gopamine, but an agonist.

An agonist is an impersonator.

It doesn't turn into dopamine, but it's shaped just like it.

It binds directly to the dopamine receptor and tricks the cell into firing as if real dopamine were there.

The text lists a few.

Apomorphine, bromocryptine, pramapixel.

Let's start with apomorphine.

First, don't let the morphine part fool you.

It's not an opioid, it's not a narcotic.

It's a very fast -acting rescue drug for those acute -off episodes we talked about.

So like the inhaler.

Exactly.

Another option for a rescue.

Usually injected subcutaneously or taken as a film under the tongue, but the nausea, the nausea is profound.

You almost always have to pre -treat with a strong anti -medic medication.

Then there's bromocryptine.

Bromocryptine is an ergot derivative.

It's effective, but generally less so than levodopa.

We often use it in younger patients early in the disease to try and delay the need for starting levodopa or later on as an adjunct to help smooth out the on -off fluctuations.

And kevirgoline is another one.

It is, but it's rarely used now.

The text flags a really serious safety alert for cardiac valvulopathy.

It can cause fibrotic damage to heart valves.

Not worth the risk.

Not usually, no.

So we mostly see the non -ergot agents.

Pramapixel and ropineural.

Right.

They are much more common because they spare the heart valves.

But they come with their own very terrifying side effect mentioned in the text.

Sleep attacks.

That sounds sudden.

It is exactly that.

It's not just feeling drowsy.

It's an episode of falling asleep abruptly and without warning during activities of daily living.

Like while you're talking.

Or eating.

Or driving.

Driving.

Wow.

That is a massive public safety hazard.

It's huge.

Patients on these drugs have to be explicitly warned that they might literally fall asleep at the wheel with no prior warning.

It's a conversation you cannot skip.

And these drugs are also heavy hitters for the impulse control disorders we mentioned.

The gambling and the hypersexuality.

Even more so than libidopa in some studies.

The risk seems to be particularly high with the agonists.

Okay.

Let's look at the enzymes.

We're trying to keep the dopamine we have around for longer.

Section 6 covers the enzyme inhibitors.

MAOB and COMT.

Think of these as the cleanup crew prevention.

The brain has these enzymes that are constantly naturally sweeping up and breaking down dopamine.

If we can handcuff the cleanup crew, the dopamine gets to stay on the dance floor and work its magic for longer.

Great analogy.

First up, the MAOB inhibitors.

Sleduline is the prototype here.

MAOB, which stands for monoamine oxidase B, is an enzyme that specifically breaks down dopamine in the brain.

Sleduline blocks it.

Okay.

By doing that, it can prolong the action of the dopamine that's there.

And the text says it can delay the need for starting levodopa by about a year.

But with any MAO inhibitor, we have to talk about the cheese effect.

This is legendary in pharmacology.

The tiramine interaction.

You have to know this one.

See, there's another enzyme, MAOA, that lives in the gut, and its job is to break down a substance called tiramine.

Tiramine is found in things like aged cheese, red wine, cured meats, bananas.

All the good stuff.

The entire charcuterie board, basically.

Normally, MAOA handles it, no problem.

But at high doses, sleduline loses its specificity for MAOB and starts blocking MAOA too.

And what happens then?

If you eat that cheese or drink that wine, the tiramine isn't broken down.

It builds up in your system and triggers a massive catastrophic release of norepinephrine.

Which causes?

A hypertensive crisis.

Blood pressure goes through the roof.

It's stroke territory.

It's a medical emergency.

So if you are on high dose sleduline, you have to put down the cheddar.

You do.

Resaguline is the newer cousin.

It's more potent and a more irreversible inhibitor.

And it's generally safer regarding the tiramine risk at normal doses.

But the text still advises caution, especially at higher doses.

Now the other enzyme family.

COMT inhibitors.

The drugs are Tolkapone and Entacapone.

COMT stands for catechol -O -methyltransferous.

It's just another enzyme that inactivates dopamine.

These drugs inhibit it.

They are strictly levodopa boosters.

They have no effect on their own.

Their only job is to increase the amount of levodopa that stays active and gets to the brain.

Tolkapone has a scary black box warning, though.

It does.

Fatal hepatotoxicity.

It can destroy the liver.

Because of that, it's a last resort drug.

You have to monitor liver enzymes constantly.

And it's very rarely used.

So Entacapone is the preferred one, then?

Yes, absolutely.

No liver failure risk with Entacapone.

But it does have a quirky side effect.

It can turn the urine a brownish -orange color.

Again, something you have to warn the patient about so they don't get scared.

And a general note from the text that seems really important.

Since these drugs boost levodopa, they can also boost levodopa's side effects.

Right.

It's a critical point.

If you add Entacapone to a patient's regimen, you might suddenly trigger that writhing dyskinesia because you've effectively increased their dopamine dose.

You often have to lower the levodopa dose when you add an EOMT inhibitor to maintain that balance.

Rounding out the Parkinson's drugs, we have a few miscellaneous ones.

Let's start with amantadine.

Ah, amantadine, the accidental discovery.

It was actually developed as an antiviral drug for influenza prophylaxis.

No way.

Yes.

Doctors just happened to notice that their Parkinson's patients who were taking it for the flu started moving better.

Its mechanism is complex.

It's a weak antagonist of NMDA receptors.

The biggest problem is tolerance.

It works great for a few weeks or a few months, and then the effect just fizzles out.

And finally, a very specific drug for a very specific problem.

Pima vancerin.

This one addresses a real nightmare of advanced Parkinson's disease.

PD psychosis.

About 40 % of PD patients eventually develop hallucinations or delusions, but you can't give them regular antipsychotics.

Because those block dopamine and you'd make their movement impossible.

Pima vancerin is special because it treats the hallucinations without blocking dopamine receptors and worsening the motor symptoms.

But there's a black box warning here, too.

A very important one.

It's associated with increased mortality in elderly patients with dementia -related psychosis that is unrelated to Parkinson's.

So this drug is strictly for Parkinson's disease psychosis and nothing else.

Okay, that is a mountain of pharmacology.

Let's bring it to the bedside.

The nursing process for Parkinson's disease.

This is where it all comes together.

Assessment is critical.

Check for glaucoma before starting any anticholinergics.

Check for those suspicious skin lesions before starting levodopa.

Get baseline vitals lying, sitting, standing.

So you have a baseline to catch that orthostatic hypotension.

The interventions are all about safety and timing.

Timing is everything.

Parkinson's meds must be given on time every single time.

A 15 or 20 minute delay can send a patient plummeting into an off state where they can't even swallow the pills you're trying to give them.

And the diet teaching we touched on.

It's so important.

Low protein foods during the day when they need to be mobile and they can save their higher protein meal for dinner when they're settled for the evening.

Or just be diligent about separating the protein from the pills by at least an hour.

This is a major and often missed reason for drug failure.

The patient is just eating a turkey sandwich with their meds.

And home safety.

That shuffling gait makes them a walking trip hazard.

A huge one.

Remove all throw rugs.

They are the enemy.

They just catch the toe.

Install grab bars in the bathroom and hallways.

And teach them to be conscious of their walking to think, March, don't shuffle.

To consciously lift their feet with each step.

And the withdrawal warning.

You can never, ever stop these drugs, cold turkey.

You risk sending them into a rebound Parkinsonism or even neuroleptic malignant syndrome.

Even if they are sick or NPO for surgery, we have to figure out a plan.

Maybe a patch or another form to keep the dopamine coming.

All right.

Let's all take a collective breath.

We are leaving the motor track.

We are moving upstairs to the cortex to cognition Alzheimer disease.

A huge shift from a disease of movement to a disease of the mind.

The text describes Alzheimer's or AD as incurable, progressive, and neurodegenerative.

It attacks memory, reasoning, language, and perception.

Figure 20 .2 shows the core pathology.

What are we looking at inside the brain?

In Parkinson's, we lost dopamine.

In Alzheimer's, we are losing acetylcholine.

The cholinergic neurons, especially in the areas for memory and learning, are degenerating and dying.

And there is all this debris piling up.

There is.

There are two types.

You have neuritic plaques, which are clumps of a sticky protein called beta amyloid.

These form outside the neurons in the space between them.

Think of it like trash piling up in the streets, blocking traffic and communication.

And then you have neurofibrillary tangles.

These are made of a different protein called tau, and they form inside the neurons.

The internal skeleton of the cell twists, collapses, and the cell dies from the inside out.

So the cells are being choked from the outside by plaque, and they're collapsing from the inside because of tangles.

It's a devastating two -front war on the neuron.

And the end result is brain atrophy.

The brain physically shrinks.

The text lists three stages, preclinical mild cognitive impairment or MCI, and then the final stage, Alzheimer dementia.

And to get a diagnosis, you need deficits in at least two of the five areas listed.

And it's so important to remember it's not just memory loss.

The five areas are, one, the ability to acquire new information, which is why they ask the same question over and over.

Two, impaired reasoning in complex tasks, like they can't balance a checkbook anymore.

Three, impaired visuospatial abilities, which is why they get lost in their own neighborhood.

Four, impaired language, they can't find the word for pen or fork.

And five, changes in personality and behavior, like new onset paranoia or agitation.

So how do we treat this?

We can't fix the dead neurons or remove the plaques and tangles, at least not with the older drugs.

No, but we can try to maximize the function of the acetylcholine that is left.

And that brings us to the acetylcholinesterase or ACE inhibitors.

This is the exact opposite of the Parkinson's goal.

In PD, we blocked the EC.

Here, we're desperately trying to save every last molecule.

Precisely.

The enzyme acetylcholinesterase is the cleanup crew for AC.

It breaks it down in the synapse.

So if we inhibit that enzyme, the AC gets to hang around in the synapse longer, stimulating the receptors.

It's like turning up the volume on a fading radio signal.

It keeps the lights on a little brighter for a little longer.

The main drugs are Revistigmine, Dunpeazle, and Glantamine.

Let's talk about rhizotigni.

It penetrates the central nervous system very well.

A big advantage is that it comes in a transdermal patch, which is great for patients who might be resistant to taking pills or who have trouble swallowing.

That's a huge benefit.

It is.

But the side effects.

If anticholinergics make you dry, then these colonist race inhibitors must make you.

Wet.

Very wet.

S -L -E -G -E is back.

Nausea, vomiting, diarrhea are the biggest complaints by far.

The text says taking the oral form of Revistigmine with food really helps the GI upset, even if it slows down the absorption a bit.

It's a worthy trade -off.

And weight loss is a real concern with all that GI distress.

Anorexia is very common.

And in an elderly, frail patient, losing 5 or 10 pounds is a very dangerous thing.

You have to monitor their weight closely.

What about the heart?

Acetylcholine slows the heart rate down.

Yes.

So you can see bradycardia and orthostatic hypotension.

This is the nursing danger zone.

You give a drug to help their memory, but it drops their heart rate to 50.

And their BP bottoms out when they stand up.

They faint, they fall, they break a hip.

And their entire life changes for the worse.

We have to monitor their pulse specifically before giving these meds.

Dunpeazle is the other big one I see all the time.

Very common.

It has a long half -life, so it's usually taken just once a day, often at bedtime.

A common side effect to warn patients about, though, is that it can cause very vivid dreams and nightmares in some people.

Then we have a totally different mechanism.

Memantine.

This is an NMDA receptor antagonist.

It deals with a different neurotransmitter, glutamate.

Glutamate is the major excitatory transmitter in the brain.

But in Alzheimer's, there's too much of it leaking out of damaged cells.

It overstimulates the healthy neurons until they die.

A process called exciter toxicity.

It's like they're being excited to death.

Literally.

So, Memantine blocks that NMDA receptor, but in a very clever way, it kind of regulates it.

It stops all the background noise and static from the excess glutamate, so the real important signal can get through.

And this is usually for more advanced disease.

Yes.

Typically for moderate to severe AD.

And you can absolutely take it with an ACE inhibitor like Dunpeazle.

They work on completely different systems, so they can have an additive benefit.

Now, we have to talk about Section 12.

The text calls it the new frontier,

the monoclonal antibodies.

This is the stuff we're all seeing in the news.

This is the first time we've had drugs that actually try to modify the course of the disease, not just treat the symptoms.

These drugs target the amyloid plaques themselves.

Atanamab was the first approved back in 2021.

It was.

And it was a very controversial approval.

Its mechanism is to bind to the amyloid beta plaques and mark them for removal by the brain's own immune system.

It's like spray painting the trash, so the garbage truck finally comes and picks it up.

But you have to prove the patient has plaque first, right?

Yes.

With a P -span or spinal fluid test, you don't give it unless you know the target is there.

Then Lakanamab came along in 2023.

This one is really interesting.

It targets what are called protofeebles.

These are the soluble building blocks before they clump together into big insoluble plaques.

So it's trying to stop the trash from being dumped in the street in the first place.

And Donamab in 2024.

That one targets a specific modified form of amyloid that's already in the plaque, trying to clear out existing deposits.

But these drugs come with a very serious, very scary black box warning.

ARIE.

ARIE.

Amyloid -related imaging abnormalities.

This is the big risk.

Basically, when you start aggressively ripping plaque out of the delicate brain tissue, the brain can react.

You can get ARAE, which is edema or a swelling, or ARIH, which is hemorrhage, bleeding.

Bleeding in the brain.

Yes, microhemorrhages or even larger bleeds.

The patients on these therapies need frequent, routine MRIs to monitor for this.

The nurse needs to teach them the symptoms, headache, confusion, dizziness, vision changes, and to report them immediately.

It is a high -risk, high -maintenance, and incredibly expensive therapy.

Finally, let's wrap up with the nursing process for Alzheimer's disease.

Section 13.

This is where the patient -centered part of the textbook's title really shines.

You aren't just treating a brain.

You are treating a person, a family, a life that is unraveling.

Assessment includes cognitive function, obviously, but also family coping.

The family is the second patient in Alzheimer's disease.

Caregiver burnout is almost universal.

The nurse has to assess the support system.

Are they okay?

Do they need help?

A referral to the Alzheimer's Association.

Interventions.

Safety is number one.

All day long.

Wandering.

It's a huge issue.

Patients will just walk out the front door and keep walking with no sense of direction or danger.

You need secure locks, alarms, maybe a GPS tracker.

And you need to clear the pathways in the home.

Remove the throw rugs again.

The fall risk is astronomical.

Inconsistency.

Consistency is kindness for a confused brain.

Don't change the routine.

Don't move the furniture.

A confused brain relies on patterns and familiarity to feel safe.

If you break the pattern, you trigger agitation and fear.

And managing expectations with the family.

This is the hardest conversation a nurse will have.

You have to gently, compassionately explain that a drug like Dun & Paisal isn't a cure.

It's not going to bring mom back to how she was five years ago.

It might buy them six more months of better recognition or slow the decline a bit.

But the trajectory of the disease is still, unfortunately, down.

It's about quality of life, not a cure.

That's the goal.

Maximize safety, maximize comfort, and maximize quality of life for as long as possible.

We've covered so much ground today, from the motor rigidity of the substantia negra to the neurofibrillary tangles of the cortex.

Two diseases that just remind us how fragile our control over our own bodies and our own minds really is.

But also two diseases where good pharmacology and really, really good nursing care can profoundly change the daily experience of the patient and their family.

Whether it's timing the levodopa perfectly so they can walk to the dinner table with their grandkids or catching the bradycardia before the Alzheimer's patient falls and breaks a hip.

That's the job.

That's the art and science of it.

Understand the molecules so we can protect the person.

Thank you so much for listening to this deep dive into Chapter 20.

It's heavy material, but it is so, so essential.

Stay curious and please stay safe out there.

This has been the Last Minute Lecture Team.

Eww.

Signing off.

Boo.