Chapter 12: Introduction to Psychotropic Drugs

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Welcome back to the Deep Dive.

Today we are strapping in for what might be the most

essential mental workout of the semester.

I think so, yeah.

We're tackling a subject that I think for a lot of nursing students, and let's be honest, even for seasoned pros,

it feels a bit like trying to climb Mount Everest without oxygen.

It is definitely the steep part of the learning curve for sure.

We are diving into chapter 12 of Psychiatric Nursing, seventh edition.

The title is Introduction to Psychotropic Drugs,

and I can already hear some of you groaning, you hear pharmacology, and you've pictured these stacks of flashcards, chemical structures,

endless lists of side effects.

It is a dense topic.

There's no getting around that, but it's also probably one of the most critical tools in the psychiatric nurses toolkit.

I mean, you cannot do this job safely without understanding this chapter.

Absolutely, and the text starts with this really vivid, almost aggressive image.

It does.

It describes the United States as a drug -taking society, and they aren't pulling any punches here.

They're not just talking about illegal stuff.

No, not at all.

They're talking about the culture of pills.

It's a pervasive mindset.

The text points out that people take pills to sleep, pills to wake up, pills to lose weight.

Pills to fix emotional problems.

Right.

It feels like we are looking at a culture that believes there is a chemical fix for every single human experience.

And specifically for our context,

you know, for nursing students, we're looking at drugs used to fix mental and emotional problems.

We are talking about drugs for delusions, drugs for runaway thinking, drugs to just - To just calm your nerves when the world gets too loud.

Yeah.

And before we even get into the mechanics of how these drugs work, which we will, and we're going to make it make sense, the authors lay out a specific mission for this deep dive.

They do, and I think it's really important.

They want to move students away from rote memorization.

You know the drill?

Memorize the drug name, memorize the side effect, pass the test, and then just flush it from your brain.

Which is the worst way to learn pharmacology.

It's a trap.

A total trap.

If you rely on memorization, you are just a walking list.

The goal here is understanding why these drugs work.

If you understand the principles, the mechanics of how the body handles the drug and how the drug talks to the brain,

you don't have to memorize every single interaction.

Because you can predict them.

You can predict them.

You can look at a situation and say, oh, okay, based on the physiology, I know what's going to happen next.

It's a much deeper level of understanding.

That sounds infinitely better.

But before we get to the chemistry,

there's this fascinating warning right at the start.

They quote, Hippocrates.

Above all, do no harm.

It's a grounding moment, isn't it?

It really is.

The authors are clearly proponents of psychopharmacology.

They believe these drugs help people.

But they list six really critical caveats that every needs to internalize.

It is a reality check before we even think about opening the med drawer.

Let's run through those because I think they set the tone for the whole chapter.

The first one is blunt.

Drugs aren't always warranted.

Right.

Just because a patient is struggling doesn't mean a pill is the answer.

Sometimes the distress is situational.

Like grief.

Exactly.

Maybe they're grieving.

Maybe they just lost a job.

Maybe it's behavioral.

You know, writing a script isn't the automatic solution to human suffering.

The second caveat is even tougher to swallow.

I think drugs aren't always effective.

That's so hard to hear, especially when you want to help someone so badly.

You give them the treatment, you follow all the protocols, and sometimes nothing happens.

Or not enough happens.

Yeah.

Or not enough.

The brain is just so complex and our tools,

they aren't perfect.

Which leads right into the third point.

The best outcomes usually involve co -administration.

That means drugs plus something else.

Typically counseling or psychotherapy.

The pill might lower the volume on the anxiety, for example.

But it doesn't teach you how to cope with stress.

It doesn't fix the underlying trauma.

So the pill rarely fixes the whole problem in isolation.

Very, very rarely.

It's not a magic wand.

And speaking of magic wands, the fourth caveat is really interesting.

It says drugs can be used to avoid the hard work of getting better.

And that is a very human tendency.

Dealing with trauma, changing behavioral patterns, learning new coping skills.

That is exhausting work.

It's painful.

It is painful.

And sometimes both patients and, frankly, clinicians can fall into the trap of using medication to bypass that heavy lifting.

Just give me something to make me feel normal, rather than doing the work to be healthy.

Okay.

And then we have the physical risks.

Caveat five.

Side effects can be life -threatening.

We aren't just talking about a dry mouth here.

No, not at all.

We're talking about serious systemic reactions,

organ failure, hypertensive crises,

severe skin reactions like Stevens -Johnson syndrome.

These are potent chemicals we're introducing to the body.

And finally, number six, finding the right regimen is often trial and error.

Which is incredibly frustrating for the patient, you can imagine.

Try this.

Oh, didn't work.

Okay, try this.

It feels like we're just guessing.

Yeah, throwing darts at a board.

But because everyone's biology, their metabolism, their receptor sensitivity is slightly different, it's often the only way to find the perfect match.

So keeping all those warnings in mind, let's look back in time for a second.

The text has this great box, box 12 to 1, on the history of these medications.

I love this part.

And it divides it into two eras.

The first one is the era of serendipity, basically from 1949 to the 1960s.

Serendipity is such a polite way of saying happy accidents.

A lot of the foundational drugs in psychiatry weren't designed for psychiatry at all.

Like what?

What are some examples?

Well, take MAO inhibitors.

These are powerful antidepressants.

But they were originally discovered because a drug used to treat tuberculosis was found to improve the patient's moods.

Wait, really?

Yeah.

The doctors noticed the patients were happier, more euphoric, even though their lungs were still struggling with TB.

That is wild.

Your lungs are bad, but you seem great.

Exactly.

Or lithium, that was discovered in Australia in 1949, almost by chance.

Chlorpromazine, the very first antipsychotic, was being investigated for surgical use in France to prevent shock.

We just stumbled into the first generation of treatment.

But then the text shifts to the modern era, the 1990s to the present, and this feels much more intentional.

Much more.

This is where we see the development of the SSRIs, like Prozac.

We see the atypical antipsychotics, like Clozapine, and we start seeing drugs designed specifically for Alzheimer's.

So what's the big difference?

The big difference here is that the early drugs had a lot of clones, you know, slightly different versions of the same chemical structure.

The modern era brought agents that were substantially different in how they worked.

We moved from sort of stumbling in the dark to actually designing keys for specific locks in the brain.

Okay, so we have these powerful tools.

Where does the nurse fit in?

The text mentions the least restrictive alternative.

What does that mean in terms of pharmacology?

It's a core legal and ethical concept in psychiatric care.

Historically, if you had a severe mental illness, you were institutionalized.

Locked away in asylums.

Right.

Sometimes for life.

Psychotropic drugs changed that.

They reduced symptoms, the aggression, the psychosis enough that patients could live in the community.

That is the least restrictive environment.

The drugs are, in many ways, the key that unlocks that institutional door.

That puts a tremendous amount of responsibility on the nurse.

It does.

The nurse is the 24 -hour presence.

The doctor prescribes the medication, but the nurse is the one there at 2 in the morning.

Right.

The nurse is the one assessing, is the drug working?

Are the side effects manageable or are they becoming dangerous?

You are the eyes and ears.

You are the one who notices the subtle changes that might signal a problem.

And to help us be those eyes and ears,

the text introduces Norm's notes.

I love Norm.

Norm is great.

Norm seems to be the voice of study strategy here.

He is.

He's one of the authors.

And he pops up to give this really practical advice.

And his big advice here.

Repetition, repetition, repetition.

It sounds tedious.

It does.

It is.

But it's necessary.

You're learning a whole new language.

But Norm also reiterates what we said earlier.

Do not just memorize the list.

If you understand the principles, pharmacokinetics and pharmacodynamics, you are building a foundation.

You aren't just memorizing facts.

You are learning how the machine actually works.

So let's learn how the machine works.

We're going to break this down into the two big scary P words.

Pharmacokinetics and pharmacodynamics.

Let's start with pharmacokinetics.

Okay.

Pharmacokinetics is, simply put, what the body does to the drug.

I always remember it as the kinetics implies movement.

The drug moving through the body.

That's a great way to think about it.

It's the drug's journey through the system.

We use the acronym ADME.

ADME.

Absorption, distribution, metabolism, and excretion.

Okay.

Let's start with A.

Absorption.

Absorption is getting the drug from wherever you put it.

Usually the mouth into the bloodstream.

If it doesn't get into the blood, it can't get to the brain.

Simple as that.

The text mentions a word here.

Bioavailability.

That sounds like a buzzword we absolutely need to know.

It is crucial.

Bioavailability is the percentage of the drug that actually reaches systemic circulation.

What does that mean in plain English?

Okay, so if I give you an IV drug, the bioavailability is 100%.

It goes straight into the vein.

Immediate access to the whole body.

No barriers.

No barriers.

But if you swallow a pill, it has to survive the stomach acid, it has to pass through the intestinal wall, and then it has to face a really big hurdle called first pass metabolism.

The first pass effect.

The text uses the example of busbarone or busbar.

Walk us through that because the numbers are just shocking.

They really are.

So picture this.

You swallow a pill, it gets absorbed by the GI tract, but the blood vessels from your stomach and your intestines don't go straight to the heart to be pumped everywhere.

They take a detour.

They take a detour through something called the hepatic portal vein directly to the liver.

And the liver is like a border control agent.

Its job is to filter the blood coming from the gut to catch toxins before they hit the rest of the body.

And it sees the psych drug as a potential toxin.

Often, yes, it sees it as a foreign chemical and it tries to break it down to metabolize it.

With busbarone, the liver is so aggressive that it breaks down almost all of it on that first pass.

The bioavailability is only one to four percent.

Wait, hang on.

So if I take a hundred milligram pill,

only one to four milligrams actually make it into my general circulation.

Exactly.

That is the first pass effect.

And that is why oral doses are often so much higher than IV doses.

We have to give a huge amount just to overwhelm the border patrol and get a tiny bit through to do the job.

That's incredible.

OK, so the drug has survived the liver.

Maybe it's in the blood.

Now we are at D distribution.

Right.

Now the drug needs to get from the blood to the tissues and specifically for us to the brain.

Two things really determine this.

Lipid solubility and protein binding.

We'll talk about lipid solubility when we get to the brain barrier.

But protein binding.

The text uses the Valium example for this.

This blew my mind.

It is a classic example of why a little bit of math matters in nursing.

So in your blood, you have proteins, mostly albumin.

Think of albumin like a fleet of buses circulating in your blood.

When you take a drug like Diazepam, which is Valium, the drug molecules hop on the bus.

They bind to the protein.

And while they are on the bus, can they do anything?

No, that's the key.

While they are bound to the protein, they are inactive.

They're trapped.

They can't leave the blood.

They can't enter the brain.

They can't do their job.

Only the molecules that didn't get a seat on the bus can actually work.

And for Valium, the text says it is 98 % protein bound.

That's right.

So if you take Valium, 98 % of it is just riding the bus doing absolutely nothing.

Only 2 % is actually free and active, treating your anxiety.

OK, here's where it gets scary.

What happens if I take another drug that also wants to ride that same bus?

That is the interaction risk.

That's the danger zone.

Let's say you take drug B, and it's also highly protein bound.

It competes for those same seats on the albumin bus.

So it starts kicking some of the Valium off.

It knocks some of the Valium off the protein.

Let's say Valium binding drops from 98 % to just 96%.

That doesn't sound like a big difference.

It's just a 2 % change.

It sounds negligible, but look at the active portion, the free drug.

You went from 2 % free drug to 4 % free drug.

Oh, wow.

You have mathematically doubled the active amount of Valium in the patient's system.

Just by knocking a tiny percentage off the protein.

That is wild, my god.

And that is why nurses need to check for these interactions.

You can overdose a patient without ever changing the dose of the Valium itself just by adding a competing drug.

Suddenly, the patient is overly sedated, they're slurring their words, and you're wondering why.

It's the protein binding.

That is a huge clinical takeaway.

OK.

That is distribution.

Now we get to the engine room for metabolism.

Metabolism.

This is mostly the liver again.

Its main job being to break the drug down, usually into a water -soluble form so we can pee it out later.

And this is where we meet the enzyme systems.

The text highlights two major ones, the MAO system and the CYP450 system.

Right.

Let's start with MAO.

Monoamine oxidase.

This is an enzyme that acts like a cleanup crew.

It breaks down monoamines, which are?

Dopamine, norepinephrine, serotonin, the big three.

The big three.

It's found in the liver, the intestinal wall, and in the CNS.

And the text mentions the tiramine connection.

This is a classic nursing school test question.

I remember this one.

It is.

So usually, MAO in your liver breaks down tiramine, which is a substance found in things like aged cheeses, red wine, smoked meats, pickles.

All the good stuff.

Pretty much.

But if you are taking an MAO inhibitor, an MAOI antidepressant, you have stopped that enzyme from working.

You've inhibited it.

So the tiramine doesn't get broken down.

Right.

It just builds up.

And the high levels of tiramine can cause a sympathetic crisis.

Your blood pressure shoots through the roof.

It can cause a stroke.

That is why patients on MAOIs have such strict dietary restrictions.

You literally cannot eat a pepperoni pizza or have a glass of Chianti, or you could end up in the ER.

Got it.

OK, now the other system, the CYP450 system.

First off, why the name?

The text calls it a geeky detail.

It is incredibly geeky, but kind of cool.

It stands for cytochrome P450.

P stands for pigment because it's colored.

And 450 is the wavelength of light in nanometers that it absorbs.

You don't really need to know that for clinical practice.

It explains the weird name.

It does.

What you do need to know is that these are the enzymes that chew up most psych meds.

And there are a bunch of them.

Correct.

There are families of them.

The text mentions CYP1A2, CYP2D6, CYP3A4.

Think of them as different assembly lines in the liver factory, each specialized for certain types of drugs.

And this leads to the smoking connection.

This was the most practical clinical pearl in the whole chapter for me.

It is absolutely vital.

Tobacco smoke, specifically the hydrocarbons in the smoke, not the nicotine acts as an inducer for the enzyme CYP1A2.

Inducer means it makes the enzyme work faster.

It speeds it up.

Exactly.

It revs up the engine of that assembly line.

So if you smoke, your liver is chewing up drugs metabolized by 1A2 really, really fast.

The text uses the example of Alanzapine, Zyprexa.

Let's role play this scenario.

So imagine a patient.

He lives at home.

He smokes two packs a day.

He's taking Alanzapine for his schizophrenia.

His doctor has probably set the dose pretty high, let's say 20 milligrams or more, because his liver is just shredding the drug so fast due to the smoking.

He needs that high dose just to get a therapeutic effect.

OK.

Now this patient gets admitted to a hospital unit, a locked non -smoking unit.

Right.

So he stops smoking cold turkey because he has to.

What happens to that CYP1A2 enzyme?

The inducer is gone.

The smoke is gone.

The enzyme activity slows right down to normal speed.

But he is still getting that high dose of Alanzapine.

Exactly.

The drug isn't being chewed up as fast anymore.

The levels in his blood start to rise and rise, potentially to toxic levels.

He becomes overly sedated.

Maybe he develops extra pyramidal symptoms, drooling, confusion.

And the nurse on the floor might think, oh, his schizophrenia is getting worse.

Or he's just tired from the admission.

Right.

But actually, he's toxic.

And it's all because he stopped smoking and nobody adjusted the dose.

That is a massive safety issue.

It means if a patient's smoking habits change up or down,

we have to look at their meds that are metabolized by that enzyme.

Precisely.

And the other way is true, too.

If he goes home and starts smoking again, the enzyme speeds up, his drug level plummets, and his psychosis comes roaring back.

It's a constant seesaw.

Before we move on, the text mentions a mnemonic by Dr.

McGough for antidepressants that are safe regarding these CYP interactions.

Yes.

Because the CYP450 system is so prone to these inducer and inhibitor interactions, it's really good to know which drugs don't mess with it much.

The mnemonic is, various medicines definitely commingle very easily.

OK.

That's a mouthful.

Which ones are those?

It stands for venlafaxine, mirtazapine, dezenlafaxine, citalopram,

filazodone, and acitalopram.

If you see those, you can breathe a little easier regarding CYP450 interactions.

They are sort of the friendly drugs in this specific context.

That's really helpful.

OK.

We are still in pharmacokinetics.

We have to talk about half -life.

Half -life.

The time it takes for 50 % of the drug to leave the body, it follows what we call linear kinetics.

Meaning it's consistent and predictable.

Right.

If the half -life is four hours, then in four hours, 50 % is gone.

In another four hours, 50 % of the remainder is gone.

So another 25%.

It doesn't matter if you took 10 milligrams or 1 ,000 milligrams, the timing, that percentage, is the same.

And there is a magic number here that the book points out.

Four.

Yes.

It takes approximately four half -lives to reach a steady state, which is where the amount of drug going in equals the amount of drug going out, so the level is consistent in the blood.

And also to get it out of your system.

And importantly, yes, it also takes about four half -lives to wash the drug out of your system completely once you stop taking it.

The text flags Prozac or fluoxetine.

Here's a really special case.

Prozac has a massive half -life.

It's an outlier.

Including its active metabolite nor fluoxetine, the combined half -life can be 10 days or even longer.

So if we apply that four half -lives rule.

You are looking at weeks, maybe over a month, for a complete washout of the drug from the body.

Why does that matter practically for a nurse?

OK.

Suppose you want to switch a patient from Prozac to an MAOI.

We just said MAOIs have dangerous interactions with other serotonin drugs.

Right.

If you stop Prozac on Monday and start the new MAOI on Tuesday, you still have a ton of Prozac floating around in the system.

You could trigger serotonin syndrome and kill the patient.

You have to wait for that very, very long washout period.

It's a huge safety issue.

And finally, last letter, E for excretion.

Getting it out of the body, usually the kidneys.

The big takeaway here is kidney disease and age.

If your kidneys aren't working well, you can't pee the drug out so it stays active longer.

Lithium is the classic example, right?

The classic example.

Lithium is a salt and the kidneys handle it just like sodium.

If your kidneys are struggling, maybe due to age or disease, lithium toxicity becomes a very real and very dangerous risk very quickly.

OK.

That is ADME.

We have survived pharmacokinetics.

Now we flip the coin to pharmacodynamics.

This is what the drug does to the body.

This is where we talk about the target.

The receptors in the brain, the whole lock and key mechanism.

We have agonists and antagonists.

It's a simple concept at its core.

An agonist activates the receptor.

It mimics the natural chemical.

It puts the key in the lock and turns it.

And an antagonist.

An antagonist blocks the receptor.

It parks in the spot and prevents the natural chemical from getting in.

It's like putting gum in the lock.

Nothing can get in.

But the body isn't static, right?

It adapts to this.

And the text talks about down regulation.

This explains one of the biggest mysteries for patients.

Why does my antidepressant take a month to work?

It is a great question.

If an antidepressant increases serotonin levels in the synapse immediately, which it does, why don't you feel better immediately?

Exactly.

If the chemical is the fix, the fix should be instant.

It's a logical question.

The leading theory is down regulation.

When you chronically flood the brain with extra serotonin, the receptors on the other side say, whoa, this is too much noise.

It's too loud in here.

So they protect themselves.

They protect themselves.

They actually decrease in number or they become less sensitive over time.

And this process of remodeling the receptors seems to take about two to four weeks.

So the mood improvement might actually be caused by the receptors changing their structure or number, not just the raw increase in the chemical.

That is the leading theory, yes.

We're waiting for the brain to remodel its own receiving equipment.

The drug is just the catalyst for that remodeling process.

The other side of that adaptation is pharmacodynamic tolerance.

The text uses the alcoholic example, and this is frankly terrifying.

It is, but it explains so much about addiction.

A chronic heavy drinker might have a blood alcohol level of 0 .35.

Which for a non -drinker?

For you or me, we'd be comatose or dead.

This person is walking and talking, maybe a little unsteady, but functional.

Why?

Because their receptors have become desensitized.

They've down regulated.

They have tolerance.

But there is a huge deadly catch.

A huge catch.

You develop tolerance to the buzz and the sedation.

You do not develop tolerance to the respiratory depression.

The part of your brain that tells you to breathe, the brain stem, doesn't get tolerance.

So the gap between the dose that makes you feel high and the dose that makes you stop breathing gets narrower and narrower.

That's it exactly.

They need more and more alcohol to feel the buzz, bringing them closer and closer to the lethal dose for their lungs.

That is why people with very high tolerance can suddenly die of an overdose.

The safety margin has all but disappeared.

That is a very sobering realization.

Okay, moving on.

We need to talk about the bouncer at the club.

The blood -brain barrier, the BBB.

The brain is the VIP section of the body.

It has to have a constant, stable environment.

It can't have every random chemical from your lunch floating around in there.

The blood -brain barrier keeps all the riffraff out.

The text describes three dimensions to this barrier.

Anatomic, physiologic, and metabolic.

Right.

Anatomically, the capillaries in the brain are super tight.

There are no gaps like in the rest of the body.

Physiologically, there are special transport systems that decide who gets in.

But the most important rule for entry for most of our drugs is lipid solubility.

Lipid solubility is king.

It really is.

If a drug is soluble in lipids, which are fats, it can pass through the cell membrane easily.

Think of it like a ghost walking right through a wall.

What are some drugs that are really lipid soluble?

The ones you hear about.

Heroin, Valium, alcohol, nicotine.

They are highly lipid soluble.

That means they dissolve right through the membranes and hit the brain almost instantly.

That's also a big part of why they're so addictive.

That immediate, powerful effect.

What about water -soluble stuff?

Stuck outside the club.

The text has a great comparison between penicillin and dopamine.

Penicillin is water -soluble.

It doesn't cross the barrier well.

And that's great because you can give massive doses of penicillin for an infection in your leg and it won't mess up your brain chemistry.

But what about dopamine?

If a patient has Parkinson's, we know they're low on dopamine.

Why can't we just give them a dopamine pill?

Because dopamine itself also doesn't cross the barrier well.

It's mostly water -soluble.

And if you were to give a huge dose to try and force it in, that dopamine would hit the heart and blood vessels first.

The peripheral effects.

You'd cause a heart attack long before you ever helped the tremor in the brain.

So that is why we use levodopa instead.

Yes.

Levodopa is a precursor molecule.

It can cross the barrier.

It's like it has a VIP pass.

Once it's safely inside the brain,

enzymes convert it into dopamine.

It's a Trojan horse.

We sneak it in and then it does the work where it's needed.

There is another player at the barrier.

The p -glycoprotein aflux transporter.

The text calls this the ferry system.

I call it the bouncer.

This transporter's job is to grab drugs that have managed to sneak into the cell and physically throw them back out into the blood.

You're not on the list, get out.

This explains why second -generation antihistamines don't make you sleepy, right?

Like Claritin versus Benadryl.

Exactly.

The old ones, like Benadryl, got into the brain and stayed there.

Major sedation.

The new ones, like loratadine, get into the brain.

But this p -glycoprotein bouncer grabs them and kicks them out immediately.

So they treat your allergy in the body, but they don't sedate your brain.

But what if another drug inhibits this transporter, ties up the bouncer?

Then the drug that was supposed to be kicked out gets in and stays in.

This can raise the drug levels in the brain significantly, even if the blood serum levels don't change.

It is another hidden and potentially dangerous interaction.

Let's zoom in even further.

We are inside the brain now.

Let's talk neurobiology.

Just the basics.

The basics.

Neurons.

You have the dendrites, which are the receivers, the cell body, and the axon, which is the sender.

And between the axon of one neuron and the dendrite of the next is the synaptic cleft, the tiny gap where the chemical message has to jump across.

And the text makes a point to note that arborization, the branching of these neurons, continues into early adulthood.

The brain is still building itself.

Which is why drug and alcohol use in adolescents and young adults is such a major concern.

The construction site is still active.

Messing with the chemistry during that period can have long -term structural effects on how the brain is wired.

Okay, let's talk about the messengers, the neurotransmitters.

Table 12 -3 lists the big ones.

Let's run through them because understanding these is really understanding the diseases.

First up, dopamine.

Dopamine is the Goldilocks chemical.

Too much.

You get schizophrenia, psychosis, hallucinations.

Too little.

You get Parkinson's disease with tremors and rigidity.

And it's also implicated in depression.

It regulates movement, reward, and reality testing.

Serotonin.

That's the mood regulator.

Low serotonin is the hallmark of depression.

Most of our common antidepressants are trying to boost this chemical in some way.

GABA.

GABA is nature's Valium.

It's the primary inhibitory neurotransmitter.

It calms things down.

It tells neurons to stop firing.

So low GABA means anxiety.

The brain is firing too much.

It's overactive.

Most anti -anxiety meds like benzodiazepines work by boosting GABA or helping it work better.

And acetylcholine.

That's involved in memory, learning, and muscle movement.

And clinically, low acetylcholine is strongly associated with Alzheimer's disease.

So we have the chemicals, the messengers.

Now they have to hit the lock, the receptors.

The text distinguishes between the first messenger and second messenger systems.

What's the difference?

Think of the first messenger system or lying in gated channels as a doorbell.

You press the button and the door opens immediately.

A neurotransmitter binds and an ion channel for sodium, calcium, or chloride snaps open.

It happens in milliseconds.

GABA works this way.

It's fast, immediate inhibition.

Stop firing now.

And the second messenger system, the G protein one.

That's more like sending a memo to the corporate office.

It's slower.

You activate the receptor on the outside, which then activates a G protein on the inside, which then triggers an enzyme, which then creates a second messenger chemical inside the cell.

It's a whole caspade of events.

It's a chain reaction.

It's a biological chain reaction.

Dopamine and serotonin usually work this way.

This might explain why they regulate more complex, slower developing states, like mood and thought, rather than just instant on -off reflexes.

Understanding this helps explain the side effects, too.

The text lists what happens when we antagonize or block these receptors.

There are tables for this.

12 -4, 12 -5, 12 -6.

Right.

Let's look at the common side effects.

If you block acetylcholine, you get anticholinergic effects.

We have a little rhyme for this.

Can't see, can't pee, can't spit, can't...

Well, you know the rest.

Dry mouth, constipation, blurred vision, urinary retention.

Exactly.

Everything dries up and slows down.

A lot of the older psychiatric drugs cause these side effects.

What if you block norepinephrine?

Norepinephrine helps keep your blood pressure up.

So if you block it, you can get orthostatic hypotension.

The patient stands up, their blood pressure drops, and they feel dizzy or even pass out.

And if you antagonize serotonin...

Ironically, with some drugs, you can cause depression or even suicidality.

You are blocking the body's primary happy chemical.

It shows what a delicate balance all of this is.

We have covered so much science.

But the text ends with what is arguably the most important part.

The patient.

Because none of this chemistry matters if the patient doesn't take the pill.

Adherence is the single biggest hurdle in psychiatry.

And the nurse has this critical duty to educate, but it's a real balancing act.

The text calls it balancing informed consent with unnecessary fear.

It's a perfect way to put it.

If I hand you a pill and I read you a list of 50 terrifying side effects from the drug insert, you're not going to take it.

You'll flush it down the toilet.

Of course not.

But if I don't tell you anything and you get a common side effect, you'll stop taking it and you'll never trust me again.

You have to use professional judgment.

What is common?

What is dangerous?

What does the specific patient in front of me need to know right now?

Box 12 to 7 lists the common reasons patients stop taking their meds.

Let's dig into these because they are so human.

Sexual dysfunction is huge.

It affects relationships, self -esteem, quality of life.

SSRIs are notorious for this.

And patients often will not volunteer this information.

They're too embarrassed.

You have to ask about it directly, but sensitively.

Also, emotional dulling.

What is that?

That's the I don't feel like myself complain.

I can't cry anymore.

I feel like a zombie to a patient that can feel worse than the original depression.

They'd rather feel sad than feel nothing at all.

And weight gain is another big one.

Especially with some of the atypical antipsychotics.

If you gain 40, 50, 60 pounds, that creates a whole new set of health and self -image problems.

It can lead to diabetes, high cholesterol, heart issues.

There's also the denial of illness.

The classic.

I'm not sick anymore, so I don't need the pills.

Which is actually a sign the pills are working.

But in psychiatry, when you feel better, you often think you are cured.

You stop the meds, the underlying chemical imbalance returns, and the symptoms come back.

It's a frustrating cycle of relapse.

The text also touches on safety teachings.

Obvious things like driving, machinery, pregnancy.

And we can't forget ethnicity and genetics.

The text highlights that different populations can metabolize drugs very differently.

Right.

This goes right back to that CYP450 system we talked about.

It does.

Some populations are known to be poor metabolizers of certain enzymes.

They like the enzyme or it's very slow so they can get toxic on normal doses.

Others are ultra -rapid metabolizers.

They have extra copies of the enzyme gene and they chew up the drugs so fast it has no effect.

And this often runs along genetic and ethnic lines.

It does.

So a standard dose for a Caucasian male might be a toxic dose for an Asian female or vice versa, depending on their specific CYP450 genetic profile.

We have to treat the individual, not the textbook average.

Personalized medicine is becoming more and more important here.

So bringing this all together, what is the synthesis here?

What's the big picture for the nursing student?

I think the synthesis is that psychotropic drugs are powerful, complex tools.

They aren't magic.

They rely on the basic laws of physics and chemistry, ADME, protein -minding, lipid solubility.

And as a nurse, understanding these laws is what protects your patient.

Exactly.

If you understand the first -pass effect, you understand why an oral dose is what it is.

If you understand protein -minding, you can anticipate dangerous interactions.

If you understand the blood brain derriere and half -life, you understand why we choose specific drugs and why washout periods are critical.

It moves you from just being a pill dispenser to being a real clinician.

And it reminds us of the human element.

These chemicals alter the very essence of the brain.

A person's mood, their thoughts, their personality.

That requires immense respect, education, and empathy.

The pill is just one part of the therapy.

The nurse, the therapeutic relationship, is the other critical part.

Well said.

We have unpacked the liver, the brain, and pretty much everything in between.

Hopefully, for everyone listening, Chapter 12 feels a little less like Everest and a little more like a manageable and honestly fascinating hike.

And just remember Norm's advice.

Repetition, repetition, repetition.

It really does work.

Thanks, Norm.

And thank you for listening to this Deep Dive.

Thank you from the Last Minute Lecture Team.

See you next time.