Chapter 14: CNS Stimulants & ADHD Medications

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Okay, let's unpack this.

If you're gearing up for exams or just trying to get a handle on, while some of the most potent drugs out there,

we are diving deep into Chapter 14,

Central Nervous System Stimulants and Related Drugs.

That's right.

Our mission today is sort of like giving you the ultimate shortcut.

We want to help you understand how these really powerful compounds work with the body's complex neurological checks and balances.

Yeah, we need to nail down how they work, the mechanism of action, how they're classified, because that can get a bit confusing.

It really can.

And crucially, the nursing considerations, the things that save lives when using these for ADHD, narcolepsy, obesity, even migraines.

Exactly.

All based on Lilly's Chapter 14.

So first things first, let's get our term straight.

A CNS stimulant.

Basically, it's a drug that stimulates or excites specific bits of the brain or spinal cord, speeds things up.

Got it.

And sympathomimetic.

That sounds like sympathetic nervous system.

Precisely.

Think fight or flight.

These are adrenergic and dopaminergic drugs.

Yeah.

They mimic what your sympathetic nervous system does naturally when activated.

Okay.

So how does this stimulation actually happen?

Well, fundamentally, it's about shifting the brain's balance towards excitation.

You either flood the system with excitatory neurotransmitters like dopamine, morepinephrine, serotonin, or you block the inhibitory ones that normally put the brakes on.

The chapter breaks these down in a few ways.

Chemical structure, where they act.

Yeah.

Three main ways.

Chemical structure, like amphetamines or xanthines, sight of action, like the cerebral cortex or brainstem, and probably most useful for us, the therapeutic category.

Like anti -ADHD, anti -archileptic, that kind of thing.

Exactly.

So let's stick with those therapeutic categories.

It makes the most sense for practice.

Perfect.

Let's jump into the big ones then.

Treating ADHD and narcolepsy.

ADHD, we know, involves difficulty focusing, hyperactivity, impulsivity, and the diagnostic criteria now mention symptoms by age 12.

And narcolepsy is about that overwhelming, excessive daytime sleepiness, EDS, and sometimes cataplexy, that sudden muscle weakness, often triggered by emotions.

So for both of these, CNS stimulants are the first choice.

They are.

First line treatment.

But, and this is a big, but we're talking about potent drugs here, the amphetamines and phenidates are schedule three controlled substances in Canada.

That tells you something immediately.

Right.

High potential for tolerance, dependence,

misuse.

Absolutely.

It's a major clinical concern right off the bat.

It's not just about the heart, though that's a risk.

It's the behavioral side too.

So let's talk about the heavy hitters.

Amphetamines and phenidates,

like methylphenidate, which most people know is a Ritalin.

How do they actually work?

How does making someone more awake help with ADHD versus just, well, sleepiness?

It's that classic sympathomimetic action.

They stimulate the parts of the brain involved in mental alertness, the cerebral cortex, the thalamus.

They do it by boosting the release of norepinephrine and dopamine and blocking their reuptake.

So these alertness chemicals hang around longer in the synapse, doing their job.

Okay.

So for ADHD, that longer action means better focus, less impulsivity.

Exactly.

It helps filter out distractions.

For someone with narcolepsy, it's more straightforward.

It's simply promoting wakefulness against that strong biological drive to sleep.

That difference seems really important for how you actually give the meds.

The chapter mentions preferring extended release forms, like Concerta.

Yes.

XR forms like Concerta or Ritalin SR are often preferred over immediate release or IR.

Think about it.

A once a day dose is easier to stick with.

Plus, it avoids that slump some get in the afternoon or evening with IR forms.

Better adherence, usually better outcomes.

Makes sense.

Now there's some potential confusion with the term analytics and a couple of unique drugs here.

Right.

Let's clear that up.

We have Modafinil, brand name AllerTech, used for narcolepsy.

It is a stimulant, but it's the only non -amphetamine stimulant in this specific therapeutic group, and its mechanism is different.

How so?

It seems to work mainly by reducing the effects of GABA.

GABA is the brain's main inhibitory neurotransmitter, the brake.

So less braking means more wakefulness.

It's classified as an analeptic.

Okay, interesting.

And the other one, the non -stimulant option for ADHD.

That's Adamoxetine, or Stratera.

It's a selective norepinephrine reuptake inhibitor.

Big advantage.

It's not a controlled substance.

So much lower risk of misuse or dependence.

But not risk -free, right?

There is a warning.

A critical one.

Yes, Health Canada issued warnings, updated in 2023, about the risk of suicidal thoughts and behaviors.

Especially in teens, that's a huge safety point nurses need to know.

Definitely a must -know.

Okay, so moving from stimulating the brain for focus and wakefulness,

to using drugs to influence behavior like eating.

Let's talk anorexians.

Yeah, it's a shift.

Historically, amphetamines were used for obesity, BMI of 30 or more, but they're not approved for that anymore in Canada.

Why not?

Same reasons.

Pretty much.

Safety concerns, that high potential for dependence and misuse we keep mentioning, just too risky for weight loss.

So what is used now?

Well,

this is where pharmacology takes a fascinating turn.

We go from brain -targeting drugs to one that works purely in the gut.

The main player now is Orlistat, brand name Zenical.

And it's not a CNS stimulant.

Okay, totally different approach.

How does Orlistat work then, if not on the brain?

It works locally, right in the intestines.

It basically blocks an enzyme called lipase.

Lipase is what your body uses to break down dietary fat so you can absorb it.

Orlistat inhibits it, pretty much irreversibly.

So if lipase is blocked, what happens to the fat?

It doesn't get absorbed.

About 30 % of the fat you eat just passes right through.

And that leads directly to the most common and, let's say, memorable side effects.

Right, the GI issues.

Oily spotting, gas, maybe even fecal incontinence.

Exactly.

Affects a significant chunk of patients, maybe 20 to 40%.

This is where patient education is absolutely vital.

You have to warn people what might happen, otherwise they'll just stop taking it.

It's about managing expectations and, frankly, dignity.

Wow, okay.

And if you're blocking fat absorption, are you also blocking other things?

Good question, yes.

You're blocking the absorption of fat -soluble vitamins.

So patients must be taught to take supplemental vitamins,

specifically ADE and beta -carotene, to avoid deficiencies.

And they need to take them separately from the Orlistat dose, usually a couple of hours apart.

That's a lot of crucial teaching.

Any other tips for taking anorexia?

Yeah, generally take them early in the day to avoid any potential sleep issues, even though Orlistat isn't a stimulant itself.

And definitely avoid caffeine.

The goal is steady weight loss, not getting wired from caffeine while on therapy.

Okay, let's switch gears again.

From controlling appetite to controlling pain, specifically migraines.

Right.

Antimigraine drugs.

Migraines are nasty, severe, often one -sided headaches, often with nausea, vomiting, sensitivity to light and sound.

And the understanding of what causes them has evolved, hasn't it?

Less about just blood vessels dilating.

Exactly.

The thinking now focuses more on decreased serotonin levels, leading to neuroplastic changes, maybe even central sensitization over time, especially with chronic migraines.

Which makes sense, then, that the first -line treatment targets serotonin.

Precisely.

The Triptans.

These are selective serotonin receptor agonists, or SSRAs.

The prototype drug is Sumitriptan, brand name Imatrix.

Their mechanism is targeted power.

They stimulate specific serotonin receptors 5 -HT1B and 5 -HT1D on cerebral arteries.

And stimulating those causes?

Vasoconstriction.

Powerful vasoconstriction of those cranial arteries.

This reduces blood flow and seems to decrease the release of

neuropeptides, too.

It basically shuts down the migraine process.

And this is abortive therapy, meaning you take it when the headache starts.

Yes, exactly.

It's designed to stop a migraine that's already underway, not prevent it.

Now, given that migraines often come with severe nausea and vomiting, taking a pill might be tough.

Are there other ways to take Triptans?

Oh, absolutely essential.

They come in oral tablets, yes, but also nasal sprays and subcutaneous self -injections.

These non -oral routes are a huge advantage.

They bypass the gut, which might not absorb well during a migraine, and they work much faster.

The injection can bring relief in maybe 10 -15 minutes.

Wow, that's fast.

But wait, powerful vasoconstriction.

That sounds like it could be risky for some people.

Ding ding ding.

Absolutely.

That's the critical safety flag here.

Because Triptans cause vasoconstriction, potentially even in the coronary arteries.

They're dangerous for people with heart problems?

Extremely dangerous.

They're absolutely contraindicated.

A definite no -go for anyone with serious cardiovascular disease.

Think angina, history of heart attack, coronary artery disease, or uncontrolled high blood pressure.

You just can't risk triggering a cardiac event.

That's a huge red flag for assessment.

What about the older migraine drugs, ergot alkaloids?

Yeah, drugs like ergotamine.

They were the mainstay before Triptans.

They also cause vasoconstriction, but they're less selective and have an even broader riskier side effect profile and more contraindications, like peripheral vascular disease.

That's why Triptans are generally preferred now.

Okay.

Last category then, analytics.

The respiratory stimulants.

Right.

The main players here are the methylxanthines.

This group includes caffeine, theophylline, and amyphylline.

Caffeine, like in coffee.

The very same.

Its mechanism is actually pretty neat, and it applies to the others too.

They work in a couple of ways.

First, they stimulate the parts of the CNS that control breathing, the medulla and spinal cord.

Second, they block adenosine receptors.

Adenosine.

That promotes sleep.

It does.

So blocking adenosine leads to increased alertness and wakefulness.

They also inhibit an enzyme called phosphodiesterase, which leads to more cyclic AMP, or CAM -AMP, accumulating, which can help relax bronchial smooth muscle.

Interesting.

So caffeine isn't just keeping us awake, it's doing other things too.

For sure.

Clinically, caffeine is used sometimes for its respiratory stimulant effects, especially in newborns.

But it's also famously used in combination pain relievers, like furanol.

Why add caffeine to a pain reliever?

Two reasons.

It can potentiate or boost the effect of the analgesic.

And its vasoconstrictive effect can help relieve certain types of headaches, like tension headaches.

Okay, wow.

So we've covered a lot of ground.

ADHD, narcolepsy, obesity, migraines,

using stimulants and related drugs.

Now let's tie it all together.

What does this mean for the nurse at the bedside or the practitioner?

This seems like a high stakes area.

Extremely high stakes.

So what does this all mean?

It means vigilance.

Constant assessment.

Before you even think about giving any CNS stimulant, you need a rock -solid baseline assessment.

Like what specifically?

Cardiovascular status is paramount.

Blood pressure, pulse, any history of chest pain, stroke, heart disease.

You need that baseline.

Also, a complete medication history.

And I mean complete prescriptions, OTCs, herbal supplements like ginseng or guarana, even how much caffeine they drink.

These things can interact or add up.

Right.

Those natural products can have stimulant effects too.

What about for kids with ADHD?

Critical point.

For kids, baseline height and weight are essential.

You need to track their growth patterns because these drugs can suppress appetite and potentially slow growth over time.

Plus, monitoring their mood and behavior for any changes.

Okay.

And are there any absolute never do this interactions we need to burn into our brains?

Like a five alarm fire warning.

Yes.

One huge one.

Never give CNS stimulants within 14 days of using monoamine oxidase inhibitors or MAOIs.

That's an absolute contraindication.

It can lead to hypertensive crisis.

Another major danger zone.

Combining triptans with SSRI antidepressants or MAOIs.

High risk of serotonin syndrome.

Serotonin syndrome.

That's serious, right?

Nervousness, fast heart rate, fever, muscle rigidity.

Potentially fatal.

Potentially fatal, yes.

So if your patient is on a triptan, you must check if they're also taking an SSRI or have recently taken an MAOI.

Critical safety check.

Okay.

Five alarm fires noted.

What about just practical implementation, timing, things like that?

Timing is key, especially with stimulants for ADHD or narcolepsy to avoid insomnia.

That's usually the most common side effect.

General rule.

Give the last dose of the day at least 4 -6 hours before bedtime.

Maybe even earlier for some individuals.

And the chapter mentions drug holidays.

What's the thinking there?

Right.

Periodic breaks from the medication.

Maybe on weekends or during school holidays.

It serves a couple of purposes.

First, it helps reassess if the drug is still truly needed at that dose.

And it can help minimize the development of tolerance or dependence.

Second, especially for kids, it gives their body a break and allows you to monitor their growth height and weight off the medication to see if it's impacting their growth curve.

Makes sense.

And a reminder about those extended release forms.

Absolutely crucial.

XR forms must never be crushed, chewed, or broken.

They're designed to release slowly.

Breaking them means getting the entire dose all at once, which can be dangerous, even toxic.

Swallow them whole.

Got it.

So ultimately, how do we know if these drugs are working?

What are we evaluating?

It comes back to the therapeutic goals.

For ADHD,

are we seeing less hyperactivity, better attention concentration, improved behavior for anorexians?

Is appetite control?

Is there appropriate steady weight loss for tryptans?

Is the migraine being aborted effectively?

Is the patient regaining function faster?

And, truthfully, are we achieving these goals without causing danger side effects?

That's the balance.

Okay.

So we've navigated the main classes.

ADHD narcolepsy drugs like amphetamines and amoxetine, anorexians like oralistat, anti -migraines like tryptans, and analytics like caffeine.

We've hit the mechanisms, the big warnings.

We've really covered the core of it.

The sympathomimetic actions, the unique non -stimulant mechanisms of the power of vasoconstriction.

And I think the final thought really has to be about respect for these drugs.

They offer huge benefits, right?

Helping a child focus in school, stopping a dilating migraine, that's life -changing.

But the potential for harm is always there.

The cardiac risks, the dependence potential, the need for careful scheduling, the strict controls, it all underscores how complex these agents are.

Using them safely demands constant vigilance, thorough assessment, and a really solid understanding of this pharmacology.

They're powerful tools, but they demand respect.

A powerful set of tools demanding respect.

That's a great way to put it.

We took the shortcut through the chapter, but mastering this stuff is definitely about understanding that power.

Thank you for joining us for this deep dive into CNS stimulants.