Chapter 22: Antipsychotics & Anxiolytics in Practice

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Welcome back to the Deep Dive.

We have a stack of notes here today that feels a little bit heavier than usual, both physically and honestly, metaphorically.

I agree with that.

Today, we are opening up the human mind, or at least the chemistry set that keeps it running.

We're looking at chapter 22, antipsychotics and anxiolytics.

This is definitely one of the heavy hitter chapters in the text.

We aren't just talking about blood pressure or digestion today.

We are talking about the drugs that, I mean, quite literally define reality for patients.

We are looking at the pharmacology of psychosis and anxiety.

And we are framing this deep dive with a very specific mission in mind.

We're calling this a last minute lecture.

Right.

We know the user profile here.

You might be a nursing student staring down a terrifying exam tomorrow morning, or maybe you are a clinician who hasn't thought about the difference between a phenothiazine and a non -phenothiazine in, what, a decade?

Right.

The goal here isn't just to list drugs.

It is to build a mental model.

If you can understand the physiology, the why, then all the side effects and the nursing interventions, they stop being these random facts you have to memorize.

And they start becoming logical consequences of the chemistry.

Exactly.

It just clicks.

So that's the plan.

We're going to navigate this chapter in exact order from the neuron all the way to the bedside.

But first, let's define the scope of the problem.

We're dealing with two primary categories, antipsychotics and anxiolytics.

And the terminology in the text can be a little fluid, so we should probably nail that down right now.

That's a good or psychotropics.

Neuroleptic is the older term, and it's actually quite evocative.

It basically means it seizes the neuron.

Wow.

Or, you know, modifies psychotic behavior.

Then you have anxiolytics, which are your anti -anxiety drugs.

These are often grouped with sedative hypnotics because, frankly, the line between calm and asleep is often just a matter of dosage.

There is a fascinating paradox mentioned right at the start of the text that I think just perfectly sets the tone for the high stakes involved here.

It really does.

It's the central irony of psychopharmacology.

These drugs are central nervous system depressants, right?

They're designed to manage symptoms of psychosis and anxiety.

But the text explicitly warns that if they aren't managed correctly or if the patient has what's called a paradoxical reaction, these same drugs can actually cause psychosis and anxiety.

It's a tightrope walk.

You are chemically altering the very machinery that processes reality.

That's why we can't just memorize Haldol Treat Schizophrenia.

We have to understand the neurotransmitters involved so we can spot when that balance tips too far in the wrong direction.

Let's get into the machinery.

Section one deals with the physiology of psychopathology.

The text provides a visualization, figure 22 .1, of the brain's communication network.

If we were to zoom in to the cellular level, what does this conversation actually look like?

Imagine a conversation between two people who refuse to touch each other.

You have the presynaptic neuron, that's the speaker, and the postsynaptic neuron, that's the listener.

And separating them is a tiny physical gap.

A tiny gap called the synaptic cleft.

So the signal is electrical inside the cell, but it has to become chemical to jump that gap.

Precisely.

The electrical impulse, the action potential, travels down the axon and hits the end of that presynaptic neuron.

This triggers these little bubbles, vesicles.

Think of them as little cargo ships stored in the cytoplasm to move to the cell wall and dump their cargo into that gap.

That cargo is the neurotransmitter.

And these neurotransmitters just float across to the listener cell.

But it's not random, is it?

They can't just ring any doorbell.

No, it's a highly specific security system.

The text uses the classic lock and key analogy, which is perfect for visualizing this.

The receptor on presynaptic neuron is configured in a very specific size and shape.

Only the correct neurotransmitter fits.

If dopamine floats over to a serotonin receptor, nothing happens.

It just doesn't fit the lock.

Okay, now this is the part that I think is crucial for understanding how the drugs actually work.

Once the message is delivered, the neurotransmitter doesn't just hang out there forever, right?

The system has to reset.

Correct.

If the neurotransmitter stayed in the lock, the doorbell would be ringing constantly.

The text outlines three fates for the neurotransmitter after the message is sent.

What are they?

One, it gets broken down by enzymes dissolved, essentially.

Two, it just diffuses away into the ether.

Or three, and this is the big one for pharmacology, reuptake.

Reuptake.

This is the recycling program.

It is.

The presynaptic neuron, the speaker,

literally sucks the neurotransmitter back up to use it again.

This is vital because so many psych drugs work by sabotaging this cleanup crew.

So if you block the reuptake, you leave the chemical in the gap longer, amplifying the message.

You make the signal louder and last longer.

So who are the messengers we need to worry about?

The text lists a big five for psychopathology.

The usual suspects, GABA, serotonin, dopamine, norepinephrine, and acetylcholine.

All of them play a role.

Let's focus on GABA first, since we'll be talking about anxiety later.

How would you describe GABA's role to a student who is trying to visualize it?

GABA, or gamma -aminobutyric acid, is the brain's brake pedal.

The brake pedal.

I like that.

It's an inhibitory neurotransmitter.

Its entire job is to regulate excitability, to calm things down.

If you have low levels of GABA, or if your GABA receptors aren't kicking enough of it, the brain's idle is set way too high.

And that's anxiety.

That's the When we prescribe a benzodiazepine, we are essentially greasing the brake pedal.

That's a great way to put it.

Benzodiazepines bind to the GABA receptor site and make that receptor more sensitive to GABA.

They don't replace GABA.

They just make the GABA you already have work much, much harder.

So it amplifies that braking signal.

Exactly.

It makes the brakes more effective.

Okay.

So GABA is the brakes.

Now let's look at the engine, the dopamine connection.

This seems to be the main character in the psychosis story.

Dopamine is huge.

Dopamine -containing neurons regulate cognition,

emotional responses, and motivation.

It's the gas pedal for engagement with the world.

It's what makes things interesting and important.

And the text draws a pretty clear line regarding balance here.

It's a Goldilocks situation.

It is.

Too little dopamine.

You get decreased motivation, lack of pleasure, the hallmark of depression, or even Parkinson's disease.

And too much.

But too much dopamine, or maybe a hypersensitivity to it.

That is linked directly to psychosis and schizophrenia.

The brain is over -processing, finding meaning and stimulation where there is none.

This transitions us perfectly into section two, understanding psychosis and schizophrenia.

The text gives a broad definition of psychosis as a loss of contact with reality.

That's the headline.

But clinically, we need to be more specific.

It manifests as disorganized thoughts, difficulty processing information, delusions.

Which are false beliefs, right?

Right.

Like thinking the FBI is chasing you.

Exactly.

And hallucinations, which are false sensory experiences like hearing voices or seeing things that aren't there.

It can also look like catatonia, where the patient is frozen or aggressive, even violent behavior.

Right.

And schizophrenia is the major chronic disorder where we see these symptoms cluster.

Now, for the purpose of choosing drugs, the text breaks schizophrenia symptoms down into three distinct groups.

And this is important.

This is probably the most important concept for understanding the difference between the old drugs and the new drugs.

So let's break them down.

You have cognitive, positive, and negative symptoms.

Cognitive seems straightforward, memory issues, attention deficits.

Right.

Trouble with executive function.

But positive and negative in psychiatry don't mean good and bad.

No.

And that trips people up constantly.

You have to think of math.

Positive means addition.

You are adding a shouldn't be there.

So a hallucination is a positive symptom because you're adding a sensory experience.

Precisely.

You are seeing something that isn't real.

Paranoia, agitation,

incoherent speech.

These are all added excesses of normal function.

So by that logic, negative symptoms are subtraction.

Exactly.

A loss of function.

The text mentions poverty of speech where the patient barely talks.

Blunted effect,

meaning a lack of emotional expression.

Poor self -care, social withdrawal.

The personality has been subtracted.

In many ways, yes.

The spark is gone.

The text makes a specific note that negative symptoms tend to be more chronic and persistent.

They are.

And they are much harder to treat.

Historically, the older generation of drugs, the ones we call typicals, were great at knocking down the positive symptoms.

They could stop the voices.

They could stop the voices.

But they did nothing for the negative symptoms.

So you might have a patient who isn't hallucinating anymore, but they still sit in a chair all day, unable to socialize or care for themselves.

Which brings us to the toolbox.

Section three.

Anti -psychotics mechanisms and categories.

Based on the dopamine theory we just discussed, the strategy seems obvious.

If there's too much dopamine, block it.

That is the primary mechanism of anti -psychotic drugs.

They are dopamine antagonists.

Specifically, they block the D2 receptors in the brain.

But the brain is complex.

It doesn't have a specific psychotic thoughts dopamine department and a separate movement dopamine department does it.

It uses the same chemical for different tracks.

And there's the trade -off.

This is the absolute crux of the side effect profile for these older drugs.

What happens?

When you block dopamine in the mesolimbic pathway, you reduce psychosis.

Great.

Mission accomplished.

But when you block dopamine in the extra pyramidal motor tract, you disrupt movement regulation.

So you are chemically inducing Parkinson's disease.

Essentially, yes.

We call it pseudoparkinsonism.

Tremors, rigidity, shuffling gait.

Parkinson's disease is caused by the death of dopamine neurons.

These drugs simulate that by blocking the receptors.

There is one side benefit mentioned regarding the cam receptor trigger zone.

Yes, CTZ.

This is the part of brain that controls vomiting.

It also runs on dopamine.

Ah.

So many of these anti -psychotics, you'll recognize brand names like compazine or fenugin, are also powerful antiemetics.

They stop nausea by blocking dopamine in the CTZ.

So that's why they're used post -op sometimes.

Exactly.

Okay, let's categorize.

The text divides anti -psychotics into two major groups,

typical and atypical, or first -gen and second -gen.

The typicals are the older drugs.

They have a very strong affinity for those D2 receptors.

They clamp onto them tight.

And the result of that is?

It makes them very effective against positive symptoms, the hallucinations, the delusions.

But because they hit that D2 receptor so hard, they carry a much higher risk of those extra -pure middle syndrome side effects or EPS.

The movement disorders.

Right.

And the atypicals, the second -generation drugs, they're more nuanced.

They have a weak affinity for D2, but a strong affinity for D4 receptors.

And crucially, they also block serotonin receptors.

And what's the clinical result of that weak D2 strong serotonin mix?

They treat both positive and negative symptoms.

This was the breakthrough.

Suddenly, we had something that could help with the social withdrawal, the blunted affect, and the movement side effect.

Generally much, much lower because they don't hammer that D2 receptor in the motor tract as hard.

Let's dive deeper into the older class first to understand the baseline.

Section four, typical anti -psychotics, specifically the phenophyazines.

These were the pioneers introduced in 1952 with chlorpromazine.

Before this, we really just had sedation and restraints.

The text subdivides them into three chemical groups based on their side effect profiles.

And those are?

Alephatic, paprazine, and piperadime.

Let's run through these quickly for the students focusing on the differences.

Group one,

alephatic.

The prototype is chlorpromazine.

What's the headline here?

Sedation and hypotension.

Big time.

These drugs really knock you out.

And they block alpha geneergic receptors, which causes vasodilation.

And that leads to orthostatic hypotension.

A significant drop in blood pressure when you stand up.

If you give a patient chlorpromazine, you do not let them get out of bed quickly.

They will hit the floor.

Okay, so that's alephatic.

What about group two, piperazine?

Examples include flufenazine and perfenazine.

These are the flip side.

Less sedation, less hypotension, but massive EPS potential.

These are the ones that really cause the tremors and the rigidity.

Any other key side effects?

They carry a higher risk of dry mouth, blurred vision, the classic anticholinergic effects.

And the text flags a specific blood risk here.

A granulocytosis.

Right.

A dangerous drop in white blood cells.

It's rare with these, but nurses need to be vigilant for signs of infection, like a sudden fever or sore throat.

Okay.

And group three, piperadine.

The example is theorazine.

This one is sort of a middle ground.

Strong sedation again, but low blood pressure effects and fewer EPS symptoms.

There's a catch.

A big one.

Unlike the others, this group has no antimetic effect.

It won't help with nausea at all.

Now looking at the pharmacokinetics of phenothiazines in general,

the text mentions something visually striking regarding metabolism.

Ah, yes.

The pink urine effect.

Tell us about it.

I always highlight this because it's completely harmless, but can be absolutely terrifying to a patient if you don't warn them.

Phenothiazine metabolites oxidize upon exposure to air, and they often turn the urine pink, or even a red -brown color.

Imagine not telling a patient that.

They go to the bathroom and think they are hemorrhaging.

Exactly.

It's such a vital piece of patient teaching.

Your urine might change color.

It's just the chemistry of medication.

It's not blood.

That five second conversation can prevent a massive panic attack.

What about the timeline for these drugs?

If I take a pill today, when does the psychosis stop?

It is not instant.

That's a common misconception.

You might see some sedation immediately, sure, but an observable therapeutic response takes seven to ten days.

And the full effect?

You're looking at three to six weeks.

That is a long time to wait if you're hearing voices.

It is, and it's another key teaching point.

You have to manage those expectations.

Let's look at the prototype drug for this class.

Fluphenazine.

Okay.

Fluphenazine is used for psychosis and schizophrenia.

It's highly protein bound and has a long half -life.

For patients who struggle with taking a pill every day, which is very common in schizophrenia, we have the decanoate injection.

The depo shot.

It's a depo shot released slowly from the muscle.

One injection can last up to six weeks.

It's a game changer for adherence.

Any specific iterations to flag?

Two big ones from the text.

Antacids decrease absorption, so spacing them out is key.

You can't take them together.

And cavava.

The herbal supplement.

Yes.

Patients often take cavava to relax, thinking it's harmless.

But if you mix it with fluphenazine, it dramatically increases the risk of dystonia.

It makes the muscle spasms worse.

Much worse.

We've been throwing around this term EPS a lot.

Section five is all about the major adverse reactions.

We need to define these clearly because they're classic exam questions and, more importantly,

critical clinical observations.

Extra pyramidal syndrome, or EPS.

It's an umbrella term for a cluster of movement disorders caused by that dopamine blockade.

What's under the umbrella?

First, you have pseudo -Parkinsonism.

We mentioned this stooped posture, mask -like facies, meaning the face loses expression, a shuffling gait, and the classic pill -rolling tremor of the fingers.

It looks just like Parkinson's.

It does.

Then there is acute dystonia.

This is the one you said was scary.

This is the scary one.

It occurs in about 5 % of patients, usually early in treatment, within days of starting the drug.

It involves sustained, painful muscle spasms.

The eyes might roll back in the head.

The neck might twist violently to one side.

Why is it considered a medical emergency?

Laryngeal spasms.

The muscles of the throat can seize up, compromising the airway.

The patient can't breathe.

How do you treat it?

You can't just wait for it to pass.

No.

You have to counteract the dopamine block immediately.

You usually use an IV or IM anticholinergic drug like benstropine, which is cogentin, or a benzodiazepine like lorazepam.

And that restores the balance?

It restores the balance between dopamine and acetylcholine in the motor centers and relieves the spasm.

Okay.

Next on the list is akathisia.

This is more common, affecting about 20 % of patients.

It's a profound internal restlessness.

The patient has trouble standing still.

They feel like they have to move.

They pace.

They rock back and forth.

It's intensely uncomfortable.

The danger here is misdiagnosis, isn't it?

It could just look like anxiety or agitation.

Exactly.

And this is a huge clinical trap.

If a nurse sees a patient pacing and thinks, oh, their psychosis is getting worse, they are agitated and gives more of the antipsychotic.

They make the akathisia worse.

So much worse.

You treat akathisia with a benzodiazepine or a beta blocker like propranolol, not more antipsychotic.

And the last and perhaps most tragic one, tardive dyskinesia or TD.

TD is a late phase reaction.

It usually happens after a year or more of treatment.

The text notes it's more prevalent in smokers.

What does it look like?

You see protrusion and rolling of the tongue, snacking of the lips, chewing motions, involuntary movements of the limbs and trunk.

It looks like the patient is constantly chewing invisible gum.

Misdiagnosis.

It is often irreversible.

That's the tragedy.

Once it starts, even if you stop the drug, the symptoms might not go away.

Prevention is the only real strategy.

So you have to catch it early.

You have to be doing regular screenings, aim scale to catch the very first signs and then switch meds immediately.

Moving from chronic to fatal.

Let's talk about neuroleptic malignant syndrome or NMS.

This is rare, but you cannot miss it.

It is potentially fatal.

It's a systemic collapse triggered by the dopamine blockade.

What are the red flags?

The absolute must -knows.

Sudden high fever hyperthermia.

We're not talking 100 .5.

We're talking 104 .5.

Then muscle rigidity that the text described as lead pipe rigidity.

You physically cannot move their limbs.

So fever and rigidity.

What else?

Altered mental status, confusion, stupor, blood pressure fluctuations and rhabdomyolysis.

That's muscle breakdown that floods the kidneys with protein and causes acute renal failure.

If a nurse sees this triad fever, rigidity, confusion, what is the immediate intervention?

Step one, stop the antipsychotic immediately.

Then you treat the symptoms aggressively.

4V fluids for hydration, hyperthermic blankets to cool them down, antipyretics for the fever, and a muscle relaxant like dantrolene to stop the rigidity and muscle breakdown.

It is a full -blown medical emergency.

That covers the phenolthiazines and their risks.

Let's move to section six.

Typical antipsychotics, non -phenolthiazines.

The heavyweight champ here seems to be haloperidol.

Haloperidol or halodol.

It belongs to the butyrophenone group.

And the key concept here is potency.

It is a very high potency drug.

Give us a comparison to understand the scale.

Okay.

So to get the same clinical effect as say 10 to 25 milligrams of clopromazine, you only need 0 .5 to 2 milligrams of haloperidol.

Wow.

Small dose, big punch.

Exactly.

It behaves similarly to phenolthiazines.

It's a potent dopamine blocker.

And what does that mean?

A very high risk of EPS.

A very high risk of EPS.

It's notorious for it.

But on the flip side, it has much less sedation and less hypotension than the low potency phenolthiazines.

The text details a specific administration technique for the long -acting injection, the decano.

Yes, the haloperidol decano.

It's a viscous liquid.

You have to think of it like thick oil.

So you need a large gauge needle, like a 21 gauge.

And you absolutely must use the ZTRAC method for injection.

Can you explain ZTRAC for the students who haven't done their clinicals yet?

Sure.

You pull the skin and the subcutaneous tissue to one side before you insert the needle deep into the muscle, like the ventrogluteal.

You inject the medication, wait a few seconds, withdraw the needle, and then you release the skin.

And that creates a zigzag path.

It creates a zigzag path that seals the medication deep in the muscle.

If that thick oily medication leaks back into the subcutaneous tissue, it's very irritating.

And it can cause inflammation and

the text warns, do not massage the site.

That can force the medication back out.

Also, photosensitivity is listed as a side effect.

Yes, just like with the phenolthiazines.

Patients on haloperidol need sun protection.

Sunscreen, hats.

They will burn easily.

So the typicals were effective, especially for positive symptoms, but harsh.

The side effects were brutal.

That's why the field shifted.

Section 7, atypical antipsychotics, the second generation.

These were the game changers.

As we mentioned, they treat the negative symptoms, the social withdrawal, the blunted affect, which the typicals couldn't touch.

And the safety profile regarding movement.

Much better.

Because they tap that D2 receptor more lightly and rely more on serotonin blockade, they are far less likely to cause EPS or tardive dyskinesia.

But there's the tradeoff again.

Nature demands a balance.

There's no free lunch in pharmacology.

The metabolic tradeoff.

Instead of movement disorders with these drugs, we see metabolic syndrome.

What does that include?

Significant weight gain.

And I don't mean 5 pounds.

I mean sometimes 30, 40, 50 pounds quickly.

This leads to new onset diabetes, malatus,

and dyslipidemia, which is high cholesterol and triglycerides.

So you're trading the shakes for heart disease risks, essentially.

In a crude sense, yes.

It requires a completely different kind of monitoring.

Instead of doing the AIMS scale for movement, you're checking blood sugar, lipids, and waist circumference.

Let's look at the specific agents.

Clozapine was the first.

Clozapine is a fascinating drug history lesson.

It came out in Europe in 1971, but wasn't marketed in the U .S.

until 1990.

Why the delay?

Because of a major, and I mean major, adverse effect.

A granulocytosis.

We mentioned this with the phenethyazines.

But with clozapine, the risk is much higher, isn't it?

Much higher.

It can essentially wipe out the body's immune defenses by stopping the production of granulocytes, a type of white blood cell.

It leaves the patient defenseless against infection.

So a simple sore throat could be the precursor to life -threatening sepsis.

Precisely.

That's why clozapine is reserved for severely ill patients who don't respond to other drugs.

It's the nuclear option, and the monitoring is incredibly strict.

What does that involve?

You have to monitor the WBC count weekly for the first six months, then every two weeks.

If the white count falls below 3 ,000, you stop the drug immediately.

No exceptions.

Okay, next up is risperidone.

Risperidone is safer in terms of blood cells.

It does not cause a granulocytosis, and it has a low risk of EPS and TD, especially at lower doses.

But it's not without its issues.

No.

EPS can still occur at high doses.

And you also see insomnia and significant waking.

The unique side effect for risperidone is related to prolactin.

Hyperprolactinemia.

Right.

It can cause gynecomastia, which is breast tissue enlargement in men, and other hormonal issues.

Then we have arepiprizole.

This is our prototype for the atypicals in the text.

It's unique because it acts as a partial agonist at dopamine receptors.

It sort of modulates the activity rather than just blocking it cold.

And what about interactions we should know?

Grapefruit juice is a problem.

It inhibits the CYP450 enzymes that break down the drug, which can increase blood levels to toxic ranges.

And St.

John's Wort.

Does the opposite.

It induces those enzymes and flushes the drug out of the system too fast, making it less effective.

And the text notes a black box warning here.

Yes, for suicidal ideation.

It's a critical thing to watch for, especially in younger patients when they're first starting treatment.

Finally, in this category,

Zipracidone.

The big red flag for Zipracidone is cardiac.

It prolongs the QT interval on an electrocardiogram, or ECG.

Which can lead to a fatal arrhythmia, specifically torsades to point.

Exactly.

So it is absolutely contraindicated.

If a patient has a history of QT prolongation, or is taking other QT prolonging drugs, you have to monitor the ECG before and during treatment.

Okay.

That wraps up the antipsychotics.

Let's shift gears to section eight.

Anxiety and anxiolytics.

A different set of problems, different set of tools.

Everyone experiences anxiety.

It's a normal survival mechanism.

But the text defines the disorder as excessive anxiety that is disabling.

It's not just worrying, it's physical.

It's very physical.

Sweating palms, pacing, palpitations, urinary frequency, the sympathetic nervous system, the fight or flight system, is firing on all cylinders when it shouldn't be.

And before we reach for the prescription pad, the text emphasizes non -pharmacologic measures first.

Always first.

Relaxation techniques, psychotherapy, support groups, exercise.

We don't want to medicate if we don't have to, especially given the addictive potential of some of these drugs.

But when we do medicate, the major group is the benzodiazepines.

The benzos.

These replace the older barbiturates because they are more effective, and frankly safer specifically,

there is a lower risk of death from overdose because they have a ceiling effect on respiratory depression when taken alone.

And the mechanism goes back to our friend GABA?

Right back to the brake pedal.

They enhance the action of GABA, that inhibitory neurotransmitter.

They just calm the entire brain down.

What are they used for, besides just anxiety?

Well, severe or prolonged anxiety is the main one.

But also insomnia, seizures, because they can calm that electrical storm in the brain alcohol withdrawal and for conscious sedation before procedures like a colonoscopy.

But there's a timeline restriction mentioned in the text that seems really important.

Yes.

It is recommended for short -term use only.

The book says three to four months.

Why is that?

Two words.

Tolerance and dependency.

Your body gets used to them very rapidly.

You need more of the drug to get the same calming effect.

And if you stop suddenly, the brain goes into overdrive.

The brain, which has been relying on the drug to apply the brakes, suddenly has no brakes at all.

You get rebound anxiety that's worse than the original.

Let's look at the prototype.

Lorazepam.

Lorazepam, brand name Atifon.

It's highly lipid soluble, meaning it absorbs rapidly and crosses the blood -brain barrier very quickly.

So it works fast.

It works fast, which is why it's great for an acute panic attack.

What are the contradictions?

Who should not take this?

The text highlights narrow angle glaucoma.

It can increase intraocular pressure and sleep apnea because it relaxes the airway muscles, making the apnea worse.

And interactions.

This seems like a big one.

This is the big CNS depression warning.

Do not mix with alcohol or other CNS depressants like opioids.

The combination is deadly.

One plus one equals five here.

It can and does stop your breathing.

The text also mentions smoking and caffeine.

Right.

Interestingly, smoking and caffeine can actually decrease the effects of the drug.

Why is that?

Because caffeine is a stimulant and smoking revs up the liver enzymes.

Exactly.

A heavy smoker might need a higher dose to get the same effect.

You mentioned withdrawal.

What does benzo withdrawal look like?

It looks like the worst anxiety you could imagine coming back with a vengeance.

Agitation, nervousness, tremor, muscle cramps.

And here's the real danger.

If you stop abruptly,

you can trigger status epilepticus.

Continuous seizures.

Continuous seizures that can be fatal.

This is why you must taper gradually.

Over days or even weeks.

Never stop cold turkey.

What if someone takes too much?

Let's talk about overdose.

If they're conscious and it was recent, you can use an emetic to make them vomit or activated charcoal to bind the drug in the stomach.

If they're unconscious, it's gastric lavage pumping the stomach.

Is there an antidote?

Yes.

There is a specific antidote called flumazenil.

It's a benzodiazepine receptor antagonist.

It literally kicks the benzo off the receptor and reverses the sedation.

But there's a catch, isn't there?

A huge but.

You have to be very careful.

If the patient is physically dependent on benzos and you reverse it too fast with flumazenil, you can throw them into those withdrawal seizures we just talked about.

So you use it cautiously.

Very cautiously.

And only for

benzodiazepine overdose, not a mixed overdose.

Are there options for anxiety that aren't benzos?

Yes, thankfully.

The text highlights boost boron.

Does it different?

It has a different mechanism.

It binds to serotonin and dopamine receptors.

The big advantage is that it has far fewer sedation and dependency issues than benzos.

It's not addictive.

It doesn't give you that high or that heavy sedation.

But it's not a quick fix like lorazepam.

No.

And that's key.

It takes one to two weeks to become effective.

You can't take it for a sudden panic attack.

It's for maintenance therapy of generalized anxiety disorder.

And another dietary restriction.

Grapefruit juice again.

It leads to toxicity.

The text says to limit it to eight ounces daily.

But honestly, in practice, it's just safer to tell patients to avoid it entirely while on boost boron.

We're in the home stretch.

Section nine, nursing process and clinical judgment.

How do we apply all of this knowledge at the bedside?

Okay, so assessment is step one.

You need baseline vital signs, especially blood pressure.

So you have something to compare to when you check for that orthostatic hypotension later.

And mental status, of course.

Baseline mental status.

So you can see if the meds are working or if you're seeing side effects like confusion or over sedation.

And there's a sneaky patient behavior mentioned in the text, cheeking.

Right.

Patients with psychosis, especially paranoia, may not trust you.

They might think you are trying to poison them.

So they will hide the pill in their cheek or under their tongue and spit it out later.

So as a nurse, you have to assess for noncompliance.

You stay with them, have a conversation and check their mouth after.

Sometimes liquid meds are preferred for this very reason.

You can't cheek a liquid.

Speaking of liquid meds, there's a safety tip for the nurse handling them.

Yes.

Contact dermatitis.

The liquid form of phenothiazines can irritate the skin.

You should avoid getting it on your hands.

Wear gloves when you're drawing it up and administering it.

And when diluting them.

Dilute in fruit juice to make it more palatable.

But the text specifically warns to avoid apple juice or caffeine for floufenazine.

There's an incompatibility there.

It can cause the medication to precipitate, basically turning it into sludge in the cup.

We discussed the Z -Trek method for IM injections.

What about monitoring after the shot?

Check their blood pressure about 30 minutes after the injection.

That's the danger zone for a hypotensive episode.

And always, always keep an eye out for NMS symptoms.

If your patient spikes a fever after a shot, do not ignore it.

Finally, patient teaching.

What are the key points we absolutely have to tell them before they go home?

First, you have to manage expectations.

Explain that lag time.

It might take six weeks to feel the full effect.

This isn't a cure.

It manages symptoms that prevents them from quitting early because they think it's not working.

What about lifestyle changes?

No alcohol.

Seriously, it potentiates the sedation to dangerous levels.

Smoking cessation is huge.

Why smoking?

Because smoking induces liver enzymes and increases the metabolism of these drugs.

If a patient who is stable on a dose suddenly stops smoking, their drug levels might spike into a toxic range because their liver slows down.

You might need to lower their dose.

Safety is a big one.

Huge.

No driving or operating heavy machinery until you know how the drug affects you.

And rise slowly from sitting or lying down to avoid passing out from that orthostatic hypotension.

And the bodily changes we discussed earlier?

You have to warn them.

Warn them about the pink urine with phenolthiazines so they don't panic.

You have to discuss the potential for sexual dysfunction and menstrual irregularities.

It happens.

And it's a major reason for noncompliance if you don't address it.

And the photosensitivity?

Yes.

Wear specific tip for the dry mouth.

It's a constant miserable side effect.

Hard candy, sugar -free gum, or ice chips can help stimulate saliva.

It seems small, but it improves quality of life.

And the stop signs?

When to call the doctor immediately.

A sore throat, fever, or general malaise.

Especially with clozapine.

That could be the first sign of a granulocytosis.

You tell them it's not just a cold.

It could be your immune system failing.

You need to call us right away.

Wow.

That is a massive amount of information, but we made it through chapter 22.

It's a dense chapter for sure, but think about the impact.

These drugs balance the chemicals that literally make us who we are, our thoughts, our calmness, our connection to reality.

Just to recap quickly for everyone, we're balancing dopamine and serotonin.

We're watching the shift from typicals, where the big worry is movement disorders, EPS to atypicals, where the worry shifts to metabolism, so weight gain and diabetes.

And for anxiety, we are boosting GABO with benzodiazepines, but always, always watching out for tolerance and addiction.

And one final, crucial reminder from the text, black box warning.

Anti -psychotics carry an increased risk of mortality in elderly patients with dementia -related psychosis.

They are not a catch -all sedative for an agitated grandparent.

That practice increases the risk of death, usually from stroke or infection.

That is a vital takeaway, a really important point.

And if I can leave the listeners with one final thought, it's to reflect on the polypharmacy aspect we touched on.

We talked about kava, kava, grapefruit juice, smoking, caffeine, St.

John's wort.

We often think of pharmacology as just the pill in the bottle,

but these external factors, diet, habits, supplements, they are all chemicals too.

They are all entering the same reactor vessel.

The human body.

Exactly.

A patient might be taking their prescribed meds perfectly, but a daily glass of grapefruit juice or a new herbal tea they started could completely derail their therapy or push them into toxicity.

Pharmacology doesn't happen in a vacuum, it happens in a life.

A powerful thought to end on.

Thank you to everyone listening.

This has been the Last Minute Lecture Team taking you through the deep dive.

Good luck with your exams and your clinical practice.

You've got this.

See you next time.