Chapter 8: Drugs Used in Substance Use Disorder

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Hello and welcome back to another Deep Dive.

Today, we are absolutely rolling up our sleeves.

You certainly are.

We're tackling a topic that is not only a massive public health issue, but a critical, critical chapter for anyone in the nursing field.

Absolutely.

We are looking at Chapter 8 from pharmacology, a patient -centered nursing process approach.

And the focus is strictly on drugs and substance use disorder.

It is a heavy topic, but an incredibly important one.

I think, you know, we're going to break this down systematically.

And just to set the stakes here, if you look at the sheer scope of this issue, the text mentions that the economic cost of drug use is staggering.

I saw that number.

It's almost hard to believe.

We are talking about six hundred billion dollars annually.

Six hundred billion.

That is a number that is just, it's hard to even visualize what that means.

It is.

I mean, that covers everything.

Loss productivity, health -related issues, crime, the legal system costs.

It's just a massive drain on the economy.

And that's just the financial side.

Right.

And in terms of the human impact, the text notes that over 40 million Americans age 12 and older are using tobacco, alcohol, or illicit drugs.

40 million.

That number is just wild to me.

And when you think about it, as a nurse, or really any health care professional, you are going to see this.

It doesn't matter what floor you're on.

No, not at all.

ER,

MedSurg, a pediatric clinic, working in labor and delivery.

It doesn't matter.

You are going to encounter patients with substance use disorder.

It's unavoidable.

So our mission today is pretty specific.

We aren't just talking about street drugs in a general, you know, say no to drugs sense.

Right.

We are going to walk through this chapter sequentially.

We really need to demystify the neurobiology, what is actually happening in the brain circuitry, and then get into the nitty -gritty of the pharmacology used to treat it.

Exactly.

And we have to do it without oversimplifying the science.

The text gives us a lot of specific mechanisms, adverse effects, and crucial safety alerts.

And, you know, we're going to unpack all of them.

This is about understanding the so you can keep your patients safe.

Right.

It's not about judgment.

We aren't here to judge.

We are here to understand the pharmacology.

So let's start right at the beginning with the terminology.

I feel like for a long time we heard the words substance abuse or drug dependence constantly.

It was just the standard vernacular.

It was.

But the text makes a specific point that we are shifting away from that language.

We're now using substance use disorder or SUD.

Why the is it just semantics or is there something deeper there?

Oh, it's definitely not just semantics.

It's a very purposeful shift toward precision and, I think, just as importantly, stigma reduction.

The text explains that the term abuse is no longer used because of the violence and the stigma associated with it.

It just implies a moral failing or a willful choice to do harm.

It paints the patient as a villain.

Right.

Rather than a person needing care.

It's very loaded term.

That makes sense.

And what about dependence?

That seems like a more yeah, a more medical term.

It is.

But dependence was actually a bit ambiguous.

And here's why.

You can be physically dependent on a medication like, say, a beta blocker for your heart or an antidepressant without having an addiction.

If you stop those drugs suddenly, your body reacts.

You will have withdrawal symptoms, but you aren't addicted in that pathological compulsive sense.

Right.

You're not craving your metaprol.

Exactly.

So the DSM -5, which is the standard diagnostic manual for mental health,

moved to substance use disorder to clear up that confusion and really focus on the disorder aspect of it all.

It's not just a yes or no diagnosis, right?

The text makes it clear it's a continuum.

Correct.

It's categorized based on how many diagnostic criteria the patient meets from a very specific list.

So if a patient meets two or three of the criteria, that's considered mild SUD.

Two to three is mild.

Four to five criteria is moderate.

And if you're hitting six or seven of those criteria, that indicates a severe substance use disorder.

Let's look at those criteria for a second, because that table, table 8 .1 in the text, it lists them out.

And these are really the red flags a nurse needs to be watching for during an assessment.

It's things like cravings.

Cravings are a big one, a strong desire or an urge to use the substance.

But it's also about the impact on life functioning.

The text is very clear about that.

So things like failure to fulfill major obligations at work, school or home, like missing shifts, failing classes, neglecting childcare, that kind of thing.

Exactly.

Or continuing to use the substance even when you know it's causing social or interpersonal problems.

Like, you know, my spouse says they'll leave me if I drink again and they drink anyway.

That's a classic diagnostic criterion or giving up things you used to love, right?

Giving up important social or recreational activities just to use the drug.

And the physical aspects are in there too.

I'm looking at tolerance and withdrawal.

Right.

And we really need to define those clearly because they are core pharmacological concepts.

Tolerance is defined in the book as needing markedly increased amounts of the substance to get the same effect.

The baseline has literally shifted.

OK.

And withdrawal is having those characteristic physical symptoms when you stop or, and this is key, taking the substance just to relieve or avoid those symptoms.

But, and this is a really fascinating nuance in the text,

there are exceptions to what we classify as an SUD.

I remember seeing this and doing a bit of a double take.

You're probably thinking of caffeine.

Yes,

caffeine.

I mean, if I don't have my morning coffee, I'm definitely in withdrawal.

I get the headache, the irritability, the brain fog.

It's real.

Oh, absolutely.

The withdrawal syndrome for caffeine is real and it is well documented.

But the DSM -5 does not classify excessive caffeine use as a substance use disorder.

Well, the text is clear on this.

Even though there appears to be a withdrawal syndrome with cessation, it's not categorized as an SUD because it generally doesn't cause that level of severe clinical impairment or sociopathic behavior we see with other substances.

So my crankiness before coffee doesn't count as severe clinical impairment.

Apparently not.

Not in the DSM -5 size anyway.

Interesting.

And on the flip side, there is one non -substance that is included.

Gambling.

It's the only condition in the category of behavioral addiction that's listed in the text.

So it's about the behavior, not the substance.

It's about the pattern.

It involves that continued involvement in the activity despite the substantial harm it causes.

And importantly, it activates the same reward systems in the brain that drugs do.

Okay, so we've got the definitions down.

Now, I want to get into the why.

Because it's so easy to look at addiction from the outside, especially if you haven't lived it or treated it, and say just stop.

Just use some willpower.

The just stop argument.

Right.

But the text dives into the neurobiology and it's pretty clear that once this process starts, the brain is fundamentally physically changed.

It is.

We have to stop thinking of this as purely behavioral and start thinking of it as biological.

It's a disease of the brain.

The text focuses on the brain's reward circuit, specifically in the limbic system.

The old part of the brain.

The ancient part of the brain, yeah.

It regulates our ability to feel pleasure and other emotions.

And the key player here, the absolute star of the show, is the neurotransmitter dopamine.

The feel -good chemical.

That's the one.

Now, normally, natural rewards like food or sex or positive social interactions, they cause a release of dopamine.

It's the brain's way of saying that was good for survival.

Remember that.

Do it again.

Okay.

So it's a learning signal.

It reinforces...

Exactly.

But drugs, drugs hijack that system.

They either mimic neurotransmitters or they stimulate an excessive release of them.

They absolutely flood that reward system with dopamine, leading to mood elevation or euphoria.

And that feeling is powerful.

Incredibly powerful.

That euphoria provides an incredibly strong motivation to repeat the experience.

It hijacks that learning signal and makes it a thousand times louder.

But why does it stop feeling good over time?

I mean, we hear about people chasing the dragon, right?

Trying to get that first high back and never, ever getting there.

That's the process of remodeling.

That's the term the text uses.

With repeated use, the brain tries to adapt to this unnatural, massive flood of dopamine.

It essentially says, whoa, way too much noise in here.

We need to turn the volume down.

So what does it actually do?

It actually remodels the neural circuitry.

It reduces the responsiveness of the dopamine receptors.

It can even reduce the number of receptors.

So you basically have fewer receptors listening for the signal, like putting in earplugs.

That's a great analogy.

Exactly.

That's the biological basis of tolerance.

You need a larger dose to get the same effect because your receivers are turned down.

Okay.

That makes sense.

But here is the tragic part.

And the text highlights this specifically because the baseline is reset, natural rewards, those things that used to make you happy, like a good meal or hanging out with friends, they no longer register.

They don't provide enough of a signal.

They don't produce enough dopamine to be felt by those desensitized receptors.

So the world becomes gray.

So without the drug, the person isn't just normal.

They are in a deficit.

They're below baseline.

Right.

They experience depression, anxiety, irritability, a total inability to feel pleasure.

That's called anedonia.

They need the drug just to feel okay, not even to feel high anymore.

They're just treating their own withdrawal at that point.

That's what a lot of it becomes.

Yes.

The text also mentioned something called epigenetics.

This is a newer field that I feel like keeps popping up in our deep dives.

It's really changing how we see things.

It's where a lot of the cutting edge research is heading.

Epigenetics is the study of how environmental influences affect our genetics.

The text notes studies have shown drug use can actually alter DNA proteins,

specifically the ones that affect gene expression and function.

So it's not changing the gene itself, but how the gene is read.

Exactly.

The environment and the drug use change the way the genes work, which in turn influences drug -seeking behavior.

So it's literally rewriting the instruction manual in the cells.

That explains why willpower is often an insufficient treatment plan.

Right.

You can't just will your DNA to change back.

Precisely.

We are treating a biological change, not just a bad habit.

This is why pharmacology is so central to treatment.

Which is a perfect transition.

Let's get into the first major substance category and probably the most ubiquitous one, alcohol.

The text calls it alcohol use disorder or AUD.

It's everywhere.

It is completely woven into the fabric of our culture.

People drink to socialize, to relax, to celebrate.

But for some, it becomes a disorder.

A very serious one.

And because it's so common, the text really emphasizes screening.

This is a huge part of the nursing role.

You cannot treat what you don't identify.

And so many people hide it.

They do.

There's a graphic in the chapter, figure 8 .1, that breaks down the screening and brief counseling process.

It's four simple steps.

I think we should walk through them because this seems like a protocol every nurse should have in their back pocket.

I agree.

Step one is simple, but, you know, it's often skipped.

Ask.

You have to ask patients about their drinking.

And you do this with everyone, not just people you suspect have a problem.

It should be a universal screening question.

How do you ask without sounding accusatory or judgmental?

You use validated screening tools.

Or you simply ask in a very matter of fact way, just like you'd ask about their diet or exercise.

How many times in the past year have you had five or more drinks in a day?

Okay.

So step two is talk in plain language.

Yes.

And this part is crucial.

You discuss what they think is good and not so good about their drinking.

It's non -judgmental.

You're not lecturing.

You aren't saying you need to stop because it's bad for you.

You're exploring their perception of it.

Exactly.

You're opening a dialogue.

And step three.

Provide options.

Ask them if they want to stop or cut down or seek help.

You come up with a plan with them.

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

It's collaborative.

Not prescriptive.

No.

And step four.

Close on good terms.

Regardless of their response, you keep that therapeutic relationship open.

You let them know you are there when they are ready.

You don't burn the bridge.

I love that.

It's so respectful of patient autonomy.

Now, when we talk about drinking, we have to be specific about the math.

Oh, absolutely.

Because one drink means very different things to different people.

Box 8 .1 in the text defines a standard drink.

And I think this is where a lot of patients and maybe even some of us get it really wrong.

The math is critical because patients will say, oh, I only have two beers a night.

But if those beers are 20 ounce craft IPAs, that's not two standard drinks.

Not even close.

So what is the standard?

A standard drink contains 10 grams of alcohol.

That's the magic number to remember.

Okay.

10 grams.

What does that look like in a glass?

So it's 10 ounces of beer at 5 % alcohol.

It's 3 .25 ounces of wine at 12%.

Or it's one ounce of hard liquor at 40%.

That's 80 proof.

Wait, hold on.

3 .25 ounces of wine.

That is a very small pour.

My wine glasses at home hold way more than that.

It is a tiny pour.

Most restaurant pours are five or six ounces.

So that one glass of wine you have with dinner might actually be two standard drinks by the medical definition.

That's eye opening.

And why does that specific amount matter physiologically?

Because the liver is the bottleneck.

The text states the average person can only metabolize about 10 grams of alcohol per hour.

One standard drink per hour.

So if you drink more than that, 10 grams in an hour, it just backs up in your bloodstream.

Exactly.

It accumulates leading to intoxication and toxicity.

The liver is working at what's called zero order kinetics here.

It has a fixed speed.

It doesn't speed up just because you drink more.

It's like an assembly line with a set pace.

Okay.

That makes so much sense.

Yeah.

Let's move to treatment.

For a patient with alcohol use disorder who wants to stop or has stopped, we have what I call the big three medications listed in the text.

This is the core pharmacology.

The big three, yeah.

The first one is desulfurum.

This is the one that works on a version, right?

The negative reinforcement drug.

Yes.

Desulfurum.

The brand name is Antibuse.

It's a classic, but it is intense.

It works by inhibiting an enzyme called aldehyde dehydrogenase.

Okay.

Walk us through the chemistry there.

What does that mean?

Normally when you drink alcohol, your body breaks it down into a substance called acetaldehyde, which is actually very toxic.

That's what causes hangovers, right?

It's a big part of it, yes.

Then the enzyme aldehyde dehydrogenase quickly breaks that acetaldehyde down into harmless acetate.

Desulfurum stops that second step.

It blocks the enzyme.

So you get a buildup of the toxic stuff.

A massive buildup of acetaldehyde in your system.

And that does not feel good.

Not at all.

It's called the desulfurum reaction.

Within about 10 minutes of drinking any alcohol, the patient will experience nausea, severe vomiting, a pounding headache, chest pain,

difficulty breathing, sweating, confusion.

It feels like they're having a heart attack.

It feels like they are dying.

So the whole point is to make the patient afraid to drink.

Essentially, yes.

It's aversion therapy.

It keeps them from drinking because they know the consequences are immediate and severe.

It removes that impulsive element.

And this is the huge nursing implication.

It's not just about drinking a beer.

No.

This is where patient education is a life or death matter.

We have to warn them about hidden alcohol.

Right.

The text lists things like mouthwash.

Most Listerine has alcohol.

A lot of it.

And cough syrup, vinegar, cider, extracts like vanilla extract used in baking, some sauces, desserts cooked with alcohol like tiramisu or rum cake.

What about on the skin?

Even after showed or rubbing alcohol if it's applied to broken skin or inhaled in large amounts, they have to become detectives and read every single label.

That is incredibly sensitive.

The margin for error is so small.

It is.

And that sensitivity lasts for up to two weeks after the last dose of Dysulphuram.

Two weeks.

So you can't just skip a pill on Friday to go out on Saturday night.

Absolutely not.

You will still get violently ill.

And there's a major contraindication, too, that we have to mention.

Patients who have taken Metronidazole, the antibiotic or Peraldehyde recently, cannot take Dysulphuram because they cause that same severe reaction.

Okay.

So Dysulphuram is the stick.

It's the punishment.

What about the others?

Let's talk about Acamprosate.

Acamprosate works completely differently.

It's a GABA analog.

It helps restore the balance between neuronal excitation and inhibition in the brain, working on the GABA and glutamate systems.

Oh, it's fixing the remodeling we talked about earlier.

It's helping to remember how when you stop drinking, the brain is hyper excitable because the dampener alcohol is gone.

Acamprosate helps calm that down.

It's designed to help reduce the unpleasant feelings associated with abstinence, the anxiety, the restlessness, the dysphoria.

It's for people who are already abstinent and are trying to maintain it.

And the text mentions a very specific safety check for this one, a big one regarding the organs.

The kidneys.

You have to check the kidneys.

Acamprosate is excreted unchanged by the kidneys, so if they aren't working well, the drug will build up to toxic levels.

What's the cutoff?

It is contraindicated if the creatinine clearance is less than 30 mLmN.

Absolutely do not give it.

If it's between 30 and 50 mLmN, you have to lower the dose to 333 mg three times a day.

So as a nurse, if you see an order for acamprosate, you better be looking at that kidney function test, that GFR or CRCL.

Immediately.

It's a critical safety check.

And there's a safety alert for acamprosate regarding mental health, isn't there?

Yes.

A very important one.

You must assess for suicidal ideation before starting treatment and monitor for it throughout.

It's a rare but serious adverse effect.

Okay.

The third one is naltrexone.

Now, this one confuses people sometimes because it sounds like naloxone, the overdose reversal drug, but it's different.

Very different uses.

Naltrexone is a competitive opioid antagonist.

So how does an opioid blocker help with alcohol?

It's fascinating.

It seems that part of the pleasurable effect of alcohol is mediated through the opioid system.

So in the context of alcohol, naltrexone blocks the high.

It binds to the MU opioid receptors so that if the person drinks, they don't get that dopamine flood.

It uncouples the act of drinking from the feeling of pleasure.

So they can drink, but it just, it doesn't do anything for them.

It's like drinking water.

Essentially, yes.

It reduces the craving and it removes the reward.

But because it's an opioid antagonist, there is a massive, massive danger if the patient is also using opioids.

Huge danger.

This is a big one for exams and for real life.

If a patient is taking opioids for pain or has opioid use disorder and you give them naltrexone, you will precipitate immediate severe withdrawal.

It literally rips the opioids off the receptors all at once.

So they go from zero to 100 on withdrawal symptoms instantly.

Instantly.

It's brutal and dangerous.

The text says a patient must be opioid free for seven to ten days before starting naltrexone.

That's a critical timeline.

Seven to ten days.

Now, before we leave alcohol, we have to touch on toxicity.

The text calls acute alcohol toxicity a medical emergency.

What are we doing for that patient rolling into the ER unresponsive?

Airway management is priority one.

Always.

Alcohol suppresses the gag reflex.

They might vomit and aspirate, which can be fatal.

So airway, breathing, circulation,

the basics.

So ABCs.

Always.

We're giving IV fluids, checking glucose because alcohol can tank your blood sugar, causing severe hypoglycemia.

But there is one specific medication we give to chronic users that is absolutely essential.

Thiamine.

Vitamin B1.

Why is that so important?

To prevent Wernicke -Korsakoff syndrome, which is a form of brain damage.

Chronic alcohol use depletes the body's thiamine stores.

And without it, you get permanent neurological damage confusion, ataxia, which is a loss of coordination, and characteristic eye movement issues.

It's irreversible if you don't treat it.

It can be.

The text specifies giving thiamine 100 -milligram IM, intramuscularly, or IV to prevent this neurologic damage.

It's a standard part of what we call a banana bag in the ER.

Got it.

So fluids, glucose, thiamine, airway.

Okay, let's switch gears to the most used recreational drug mentioned in the text.

Cannabis.

Cannabis use disorder.

The text notes that while it's legal in many places now for recreational or medical use, there are still significant pharmacological effects we need to understand.

The active ingredient we're focused on is THC.

How does it work in the brain?

THC crosses the blood -brain barrier very rapidly, especially when smoked or vaped.

It binds to cannabinoid receptors, which are part of our natural endocannabinoid system.

And what does that system normally do?

It helps regulate a lot of things, like mood, appetite, pain, memory, how we respond to incoming stimuli.

The key phrase the text uses is that THC overwhelms the endocannabinoid system.

So it's too much of a good thing.

Way too much.

When it's overwhelmed, you get the classic effects.

Impaired short -term memory, balance, and coordination issues.

And in some people, especially with high doses, it can trigger significant anxiety, hallucinations, or paranoia.

There is a really important box in this chapter box 8 .2 about vaping cannabis.

I feel like this is a thoroughly modern problem that we didn't talk about in nursing school 10 years ago.

Not at all.

It's a huge issue.

The text raises alarms about the chemicals used in the vaping liquid itself, the vehicle for the THC.

We're talking about things like propylene glycol, heavy metals from the heating coils, but the one that really stands out is diacetyl.

That's the butter flavoring, right?

For popcorn.

Yes.

It gives microwave popcorn a buttery flavor.

It's generally recognized as safe to eat, but when you heat it and inhale it, it's linked to a condition called popcorn lung, which is bronchiolitis obliterans.

That sounds bad.

It is.

It's an irritant that causes irreversible lung disease.

The small airways in the lungs become scarred and constricted.

They close up.

And then there's e -volley.

E -cigarette, or vaping product, use -associated lung injury.

The text identifies vitamin E acetate as a major causative agent there.

It was being used as a thickening agent in illicit THC vape cartridges.

And what does it do?

It seems to coat the lungs, like a grease, and it interferes with surfactant and gas exchange.

So it's not just the THC, it's the delivery system that can be lethal.

Now what about medical marijuana?

The text has a box on this too, box 8 .3.

It seems to tread very carefully.

It does.

It acknowledges that many states have legalized it, but it also points to a large meta -analysis that supports avoidance in certain groups, specifically adolescents and during pregnancy.

Why adolescents?

The brain is still developing until about age 25, and heavy cannabis use can interfere with that neurodevelopment, potentially affecting things like IQ and executive function.

But it does confirm some legitimate medical uses.

Yes.

It explicitly lists cannabidiol, or CBD, for certain rare forms of epilepsy, like Dravet syndrome.

It also lists cannabis -based medicines for treating spasticity and multiple sclerosis, and for some types of chronic pain.

So it's a nuanced picture.

It's not all good or all bad.

Here is the big question for nurses, the key takeaway for a pharmacology course.

Is there a pill to treat cannabis use disorder?

We have disulfiram for alcohol.

That's the million -dollar question, and the answer is no.

The text is very clear.

There are currently no FDA -approved medications for cannabis use disorder.

Not at all.

None.

We don't have a replacement therapy or a blocker that's been proven effective yet.

So treatment relies entirely on psychosocial therapies, like cognitive behavioral therapy, CBT, and motivational enhancement.

That is a big distinction from alcohol and opioids.

A huge distinction.

Okay, let's move to what is arguably the most acute crisis discussed in the chapter, opioid use disorder, OUD.

The statistics here are just grim.

The text states that 75 % of drug overdose deaths in 2021 involved an opioid.

75%.

Three out of every four.

That is just staggering.

It is.

The mechanism here involves the Mu receptors in the brain and spinal cord.

Opioids bind to them, which does two main things.

It reduces the perception of pain, which is good for analgesia, but it also floods that reward system with dopamine, causing intense euphoria.

And the text mentions something it calls the opioid paradox.

What is that?

It's cruel, really.

In the short term, you get euphoria and pain relief.

But with long -term use, many people develop something called hyperalgesia.

Hyperalgesia.

So increased pain.

It means the patient actually becomes more sensitive to pain.

Wait, the painkiller causes more pain?

How does that work?

The nervous system becomes hypersensitive to pain signals because it's been suppressed for so long.

It's like it overcorrects.

Plus, they develop tolerance so the drug works less effectively.

So they are in more pain and the drug works less.

Exactly.

This drives them to use more or switch to stronger street drugs like heroin or, more commonly now, illicitly manufactured fentanyl.

It's a vicious cycle.

We have to talk about the rescue drug.

Every nurse, every first responder, and honestly every person should know about naloxone.

Naloxone, often known by the brand name Narcan, it is a short -acting opioid antagonist.

Pure antagonist.

Think of it as a bouncer at a club.

The opioid is currently on the receptor, causing the overdose.

It's stopping the breathing.

Naloxone comes in.

It has a stronger affinity for the receptor.

So it kicks the opioid off and it stands in the doorway, blocking it from getting back on.

And the result is immediate.

Almost immediate.

It reverses the respiratory depression, which is what kills people, very, very quickly.

The patient gasps and wakes up.

It can be given IV, IM, subcutaneously, or as an intranasal spray.

But there is a huge nursing alert here regarding the duration of action.

This seems to be one of the most important points in the whole chapter.

This is a life -or -death concept.

Naloxone is short -acting.

It wears off in about 30 to 90 minutes.

But many opioids like methadone or extended -release oxycodone, and certainly some fentanyl analogs, last much, much longer than that.

So you revive the patient.

They wake up.

They might even be angry and confused.

You high -five.

And then an hour later.

The naloxone wears off.

The bouncer leaves the doorway.

The opioid is still floating around in the blood, and it rebinds to the receptor.

The patient stops breathing again.

It's called re -narcotization.

That is a terrifying thought.

You have to monitor these patients closely.

You cannot just give the dose and send them home immediately.

The text also mentions watching for flash, pulmonary edema, which is a rare but severe reaction where fluid fills the lungs after a rapid reversal.

Okay, so that's the rescue.

Now let's talk about long -term treatment.

Medication -assisted treatment, or MAT.

The text details three main drugs.

Let's start with the oldest one.

Methadone.

Methadone is a full agonist at the MU receptor, so it acts just like other opioids, but it has a very long half -life.

And what's the benefit of that?

It satisfies the craving and prevents withdrawal for a full 24 hours.

But because of how it occupies the receptor, it also blocks the euphoria, the high of other opioids if the person uses them on top of it.

But it's highly regulated, right?

You can't just pick it up at CVS.

Not at all.

It's usually dispensed in certified opioid treatment programs, or OTPs.

Patients often have to go in daily for their dose, at least initially.

And it has a serious safety profile.

I see a boxed warning here.

A big one.

It's for QT prolongation and cardiac arrhythmias.

It can cause a dangerous heart rhythm called torsades de pointes.

So we need to be watching the EKG on these patients.

Absolutely.

A baseline EKG is often required before starting.

Next up is buprenorphine.

This seems to be becoming more common, and you can get it from a primary care provider now.

How is this different from methadone?

Buprenorphine is a mixed agonist antagonist.

It binds tightly to the MU receptor, but it only activates it partially.

It has what we call a sealing effect.

What does that mean, a sealing effect?

It means that after a certain dose, the book says usually 8 to 16 milligram taking more doesn't increase the effect.

Specifically, it doesn't cause more respiratory depression.

So it's safer.

Much safer than methadone regarding overdose risk.

And there's a clever formulation trick with this one.

It's often combined with naloxone in a sublingual tablet like suboxone.

Why would you add the rescue drug to the treatment drug?

It's a brilliant abuse deterrent.

If you take the tablet under your tongue as prescribed, the naloxone is inactive.

It's not absorbed well through the oral mucosa, only the buprenorphine works.

But if a person tries to crush the tablet and inject it to get high, the naloxone goes straight into the blood.

Exactly.

The naloxone becomes active.

It blocks the receptors and it precipitates immediate severe withdrawal.

It's designed to prevent misuse.

That is smart chemistry.

Very clever.

It is.

And the third drug for OUD is naltrexone again, which we mentioned with alcohol.

Same principle.

It's a full antagonist.

It blocks the receptor completely.

It's for preventing relapse and highly motivated people.

But again, the patient must be opioid free for seven to 10 days or you will throw them into withdrawal.

Okay, let's keep moving.

Tobacco use disorder.

The text says it affects nearly every organ in the body.

It really does.

Nicotine is a potent drug.

It stimulates the release of dopamine, norepinephrine, and GABA.

It's a powerful stimulant and relaxant at the same time.

And the withdrawal is puff irritability, hunger, difficulty concentrating, anxiety.

We have pharmacologic aids to help people quit.

We have nicotine replacement therapy, NRT.

Things like patches, gum, lozenges.

The goal there is pretty obvious.

Replace the nicotine without all the carcinogens from the smoke.

Right.

Steady state with the patch and then the gum for breakthrough cravings.

But we also have prescription meds.

Let's talk about bupropion.

Bupropion is interesting because it's actually an antidepressant, Wilbutrin.

But researchers found it mimics some of the effects of nicotine on dopamine and norepinephrine in the brain.

It helps reduce the urge to smoke and makes the withdrawal symptoms more tolerable.

But there's a major contraindication related to its side effects.

Seizures.

Bupropion lowers the seizure threshold.

So it is strictly contraindicated in anyone with a history of a seizure disorder.

Any other groups?

Yes.

It's also contraindicated in patients with eating disorders like anorexia or bulimia because the electrolyte imbalances common in those conditions already put them at a higher risk for seizures.

Then there is Varanacline, brand name Chantix.

Varanacline is a partial alpha 4 beta 2 nicotinic receptor agonist.

That's a mouthful.

It is.

Break that down for us.

Basically, it stimulates the nicotine receptor just a little bit, enough to release some dopamine and reduce cravings.

But it also sits on the receptor and blocks nicotine from binding fully.

So if you do smoke while taking it, it's not satisfying.

The reward is gone.

But this one has a very serious warning.

The black box warning.

The most serious one that FDA issues.

It has been linked to serious neuropsychiatric symptoms.

We're talking hostility, agitation, depression, and suicidality.

Even in people without a history of mental illness.

Yes, that's the scary part.

Nurses have to educate patients and their families to watch for any changes in behavior.

If they start acting out of character, become aggressive, or seem newly depressed, they need to stop the drug and call their provider immediately.

That's a heavy warning.

Let's quickly touch on the other category.

The text mentions cough and cold products.

This surprised me a bit when I first read it.

It's very common, especially among adolescents, because it's easily accessible over the counter.

Dextromethorphin, or DXM, is in a lot of OTC cough syrups.

Like Robitucin DM.

Exactly.

At recommended doses, it's an effective cough suppressant.

But at 25 times the dose, which is what is happening in robotripping,

it acts as a dissociative hallucinogen.

It works on the NMDA receptor, similar to ketamine or PCP.

And then there's purple drank or lean.

That's a prescription cough syrup containing promethazine and codeine, often mixed with soda and candy.

It's a very dangerous CNS -depressant mix.

The codeine is an opioid.

The promethazine is a sedative.

It can easily stop breathing, especially when mixed with alcohol.

What about anabolic androgenic steroids?

Hey, A .S., this isn't just about getting big muscles.

No.

The text breaks down the name.

Anabolic refers to muscle growth, and androgenic refers to male sexual characteristics.

The adverse effects are systemic, liver damage, high blood pressure, shrunken testicles, infertility.

But the text specifically highlights the psychological effect of roid rage,

extreme aggression, irritability, and paranoia.

And the withdrawal?

Is it like opioid withdrawal?

It's very different.

This is credible because it's not usually physical pain.

Withdrawal from steroids is primarily psychological.

It causes a severe deep depression that can last for up to a year.

A year.

Up to a year.

The suicide risk is very, very high during steroid withdrawal, and nurses need to be vigilant for that.

We are coming to the home stretch here, and I want to focus on the nursing role.

Specifically, the text highlights two special populations.

First, the surgical patient with an FUD.

This is a classic exam topic and a very real -world clinical issue.

If a patient has a chronic alcohol use disorder, for example, their liver enzymes are often induced.

They have something called cross -tolerance.

What does that mean for them in the OR for anesthesia?

It means they might need more anesthetic medication to stay asleep.

Their body metabolizes the drugs faster than a non -drinker.

And post -op.

That's when the real danger starts, right?

Post -op, you are on high alert for withdrawal.

Anesthesia can mask the early signs.

But if two or three days after surgery, your patient suddenly becomes tremulous, is hallucinating, and their heart rate and blood pressure spike.

You have to think about delirium tremens or DTs.

It's a medical emergency.

It can be fatal.

The second area is pain management.

This is an ethical minefield for a lot of nurses.

You have a patient with a known history of opioid use disorder, and they come in with a broken femur.

Do you give them opioids for their pain?

The expert answer and the text's answer is an emphatic yes.

Pain must be treated, period.

But aren't we worried about making their addiction worse or causing a relapse?

The text says explicitly, addressing substance use disorder is not a priority when a patient is in acute pain.

You treat the acute physiological pain with dignity.

Will they need more medication?

Yes.

You might need higher doses because of their tolerance.

You should try to avoid their specific drug of choice, if you can, to avoid triggering psychological associations.

But you absolutely do not withhold analgesia.

Withholding pain medication from these patients is unethical and it's bad medicine.

That is such an important takeaway.

Treat the patient, not the prejudice.

Finally, the chapter asks us to look in the mirror.

There's a section on the nurse with substance use disorder.

It's a reality we can't ignore.

The stats in the book show that about 1 in 10 nurses misuse drugs or alcohol.

That is roughly the same rate as the general population.

So we aren't immune just because we know the pharmacology?

Not at all.

Some would argue the risk is higher.

The contributing factors are job stress, long hours, trauma exposure,

the superhero complex, you know, ignoring our own needs to care for others, and simply access.

We are around these powerful medications all day.

What are the signs of diversion?

Diversion is when a nurse redirects a drug from a patient to themselves.

Red flags include frequent narcotic wastage, incorrect counts on the pexus machine, or patients complaining of unrelieved pain when the chart says they just received a dose of Dilaudid.

What about behavioral signs?

Isolating behaviors, frequent trips to the bathroom, mood swings in a colleague.

It's a tough situation to be in when you suspect it.

If a nurse is caught, is their career over?

Not necessarily, and the text emphasizes this.

The goal has shifted from being purely punitive to being about treatment and rehabilitation.

Most states have non -disciplinary programs.

And what do they do?

They're designed to evaluate and treat the nurse, monitor their compliance with recovery, and eventually allow them to return to practice safely under supervision.

It's about saving a life and a career, not just taking away a license.

That is a much more hopeful note to end on than I expected.

It is.

We invest so much in training nurses, we should invest in saving them too.

So we've covered a lot today.

From the dopamine reward circuit to the kidney checks for acamprosate to the half -life of naloxone, it's a lot to take in.

It is.

If I had to summarize the key takeaway for a nursing student listening, it's safety first, always.

Whether it's managing the airway in an overdose, checking for suicide risk with varenicline or during steroid withdrawal, or preventing seizures with bupropion, your primary job is to anticipate and prevent harm.

And the patient -centered approach.

Treating addiction as a chronic medical condition, like diabetes or asthma, not as a moral failing.

Exactly.

That's the whole theme.

I want to leave our listeners with a thought to chew on, something that really struck me from our conversation.

You mentioned earlier that drug use can cause epigenetic changes.

It changes how our DNA is expressed.

Yes.

That's what the research is showing.

So,

if addiction physically changes the brain's DNA and its circuitry, does that change our responsibility as nurses?

Does it mean we need to stop advocating for willpower and start advocating for long -term biochemical treatments the same way we do for diabetes or hypertension?

If the DNA itself is working differently, maybe the entire treatment model needs to be radically different too.

That is a profound question.

It definitely suggests that just saying no is, for some people,

physiologically impossible.

And perhaps our advocacy and the health care system as a whole needs to catch up to that science.

Something to think about.

Thank you so much for listening to this deep dive into Chapter 8.

It was a pleasure.

Thanks for having me.

This has been the Last Minute Lecture Team.

Stay curious and we'll see you in the next deep dive.