Chapter 22: Substance-Related & Addictive Disorders

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Okay, let's unpack this.

Welcome back to the Deep Dive.

Today, we're jumping right into the really complex world of substance -related and addictive disorders.

We're focusing specifically on chapter 22 from Varkaroules' Foundations of Psychiatric Mental Health Nursing, our goal, to really get a handle on the core ideas and how they apply in clinical practice.

And I think the absolute first place to start the foundation really is understanding what these disorders are.

Substance use disorders or SUDs, they're complex chronic diseases, they relapse.

And crucially, they are diseases of the brain.

This isn't about willpower or character flaws.

We're talking actual physical changes in brain structure and function.

These changes mess with self -control.

With decision -making circuits, it's profound.

That framing disease, not choice, changes everything, doesn't it?

How we approach treatment, how we view the person.

So over the next little while, we'll map this out.

We'll look at how diagnosis has changed with the DSM -5, touch on the neurobiology, which is fascinating, frankly.

Then we'll cover some key substances, opioids, alcohol and others.

And finally, really ground ourselves in the nursing process using alcohol use disorder as our main example.

Sound good?

Sounds like a solid plan.

Okay.

So let's start with diagnosis.

I remember back in school, we talked about substance abuse versus substance dependence, but that's changed.

It has, yeah.

The DSM -5, the Diagnostic and Statistical Manual, Fifth Edition basically combined them.

Now we have the single category, substance use disorder.

The thinking was that abuse often just slid into dependence pretty quickly.

Clinically, it made more sense to see it as a spectrum, a single disorder with varying severity.

Makes sense.

So how does a clinician diagnose an SUD now?

There are specific symptom groups they look for.

Exactly.

Four main clusters.

First, there's impaired control, using more than you meant to, wanting to cut down, but can't, spending a lot of time getting or using the substance, that sort of thing.

Okay.

Impaired control.

What else?

Then social impairment.

So use causes problems at work, school, or home.

Giving up important activities because of use, continuing despite relationship problems.

Right.

And then there's using even when it's dangerous.

That's the third one.

Risky use.

Continuing to use in situations where it's physically hazardous or despite knowing you have a physical or psychological problem that's probably caused or worsened by the substance.

And the last group covers the physical side?

Yes.

Physical effects.

This is where we see tolerance and withdrawal.

Let's pin those down.

Tolerance first.

Tolerance is basically needing markedly more of the substance to get the same effect he used to, or the flip side getting a much weaker effect from the same amount.

And what's really key with some drugs, like cocaine for instance, is how fast tolerance can develop.

It drives that cycle of escalating use very quickly.

Okay.

And withdrawal.

That seems pretty straightforward, but it's critical.

Absolutely.

Withdrawal is the set of physiological symptoms that happen when someone stops using or cuts back drastically.

These symptoms are very specific to the substance.

They can range from just feeling lousy to really severe, even life -threatening issues.

The source mentioned the origin of cold turkey.

I thought that was interesting.

Yeah.

It apparently comes from the piloerection goose bumps, like a plucked turkey's skin.

That's a really common symptom in opioid withdrawal.

Kind of makes it stick in your mind, right?

It really does.

Okay.

Before we dive into the biology, what about addictions that don't involve substances?

Yeah.

Process addictions.

Right.

Good point.

These are process addictions.

Behaviors, not chemicals, that light up the brain's reward pathways in a very similar way.

Think gambling, for example.

Gambling disorder is actually the only one officially in the DSM -5 right now, but others, like internet gaming disorder, are definitely getting a lot of clinical focus.

Just to complete the groundwork, we have to mention the legal side, the DEA schedules.

Yeah.

The Drug Enforcement Administration classifies drugs into five schedules, I through V.

It's based on their medical use potential versus their abuse potential.

Schedule I drugs, things like heroin, LSD, ecstasy, are considered to have the highest abuse potential and, crucially, no currently accepted medical use and treatment in the United States.

Contrasted with, say, schedule V.

Exactly.

Schedule V drugs have the lowest potential for abuse relative to the others and contain limited amounts of certain narcotics, like you might find in some cough preparations.

Okay, foundational concepts covered.

Let's move into the why.

Etiology.

Comorbidity seems like a massive piece of this puzzle.

The numbers are pretty sobering.

They really are.

Comorbidity or having co -occurring disorders is incredibly common.

It just means having two or more disorders simultaneously.

The statistic from 2018, 9 million adults in the U .S.

with both a mental illness and at least one SUD that tells you everything.

Wow.

9 million.

Yeah.

And it highlights why integrated treatment is so vital.

You can't effectively treat someone's depression if you're ignoring their alcohol use disorder or vice versa.

The two are often deeply intertwined.

And behind that link, there's often a strong biological predisposition, right?

Genetics.

Huge.

Genetics plays a major role.

For alcohol use disorder, heritability estimates are somewhere in the 40 % to 60 % range.

And for substances like cocaine and opiates, it can be even higher.

Maybe 70 % to 80%.

That doesn't mean you're destined to develop an SUD, but it means there's significant inherited vulnerability.

So where does this vulnerability actually play out in the brain?

Let's talk neurobiology.

Yeah.

This really reinforces the disease concept.

Absolutely.

Repeated substance use physically changes how key neurotransmitter systems work.

We're talking mainly about the opioid system, the catecholamine system, especially dopamine and the GABA system.

Dopamine is the reward chemical, right?

Yeah.

And GABA is more like the breaks.

That's a great way to put it.

Dopamine is involved in pleasure, motivation, the reward signal.

GABA is the main inhibitory neurotransmitter.

It calms things down.

Addictive substances basically hijack the brain's natural reward pathway, primarily the circuit running from the ventral tegmental area, VTA, to the nucleus accumbens.

They flood this circuit with dopamine way more than natural rewards like food or sex do.

Over time, the brain adapts to this massive surge.

It might produce less dopamine naturally or reduce the number of dopamine receptors.

So the brain changes its own structure and function.

Exactly.

The reward threshold changes.

Eventually, the person isn't taking the drug to feel good anymore, but just to feel, well, normal, or at least to avoid feeling terrible from withdrawal.

The drug becomes essential for basic functioning in a way.

And if you layer environmental stress on top of that biological vulnerability, that's often the trigger, or at least a major contributing factor.

Chronic stress from things like poverty, lack of parental supervision, exposure to violence.

It increases anxiety and negative emotions.

And for someone with that underlying vulnerability, substances can become a way to cope, albeit a maladaptive one.

It creates this really vicious cycle.

Okay, let's pivot now and look at some specific substances.

Nurses need to know the signs of

overdose,

withdrawal,

and the basic treatment approaches.

Let's start with opioid use disorder, intoxication signs.

With opioids, you'll typically see psychomotor retardation, slowed thinking, and movement.

Drowsiness is common.

A classic sign is meiosis, or pinpoint pupils, and critically decreased respiratory rate and heart rate.

And overdose.

Thesaurus stress is a key triad at the symptoms.

Yes, absolutely critical for nurses to recognize immediately.

Coma, pinpoint pupils, and respiratory depression, that's the opioid overdose triad.

Respiratory depression is what usually leads to death.

Treatment is naloxone, or Narcan, but there's a catch with its duration.

Right.

Naloxone is an opioid antagonist.

It kicks opioids off the receptors and reverses the respiratory depression very effectively.

But, and this is crucial, many opioids, especially potent synthetic ones like fentanyl, last much longer in the body than naloxone does.

So the naloxone can wear off while the opioid is still active, and the person can slip back into respiratory arrest.

That's why repeated doses and close monitoring are often essential.

Got it.

What about managing withdrawal and providing longer -term maintenance treatment?

For withdrawal, we often use medications to ease the symptoms, which can be intensely uncomfortable.

Nausea, vomiting, muscle aches, diarrhea, insomnia.

Methadone is a long -acting synthetic opioid.

It prevents withdrawal and reduces cravings.

It's tightly regulated, usually dispensed daily through certified opioid treatment programs.

Buprenorphine is another option.

It's a partial opioid agonist, meaning it activates the opioid receptors, but to a lesser degree than full agonists like heroin or methadone.

It also reduces cravings and withdrawal.

It's a schedule three drug, so it can be prescribed in office settings, which increases access.

And sometimes other meds are used just for symptom relief.

Yes, like clonidine.

It's not an opioid, but it helps manage some of the autonomic symptoms of withdrawal, like sweating, restlessness, anxiety.

Okay, switching gears now to hallucinogens.

These cause really profound perceptual changes, like synesthesia.

Exactly.

Intoxication can involve paranoia, impaired judgment, anxiety, sometimes panic.

You'll often see pupillary dilation.

And yes, synesthesia, that merging of senses like hearing colors or seeing sounds can happen.

Treatment sounds very different depending on the specific hallucinogen.

Very different, yes.

For classic hallucinogens like LSD, the often supportive.

Reassuring the person that the effects are temporary, that they're safe, reducing stimuli, often called talking down.

But, and this is a huge, but with PCP, it's a completely different situation.

PCP intoxication is a medical emergency.

Why the difference?

Patients intoxicated with PCP can become extremely agitated, unpredictable, violent, and have incredible strength.

They often experience hyperthermia.

You cannot talk these patients down.

Management requires ensuring safety.

Often physical restraints are necessary in aggressive medical treatment, usually with benzodiazepines for sedation and managing potential complications like muscle breakdown or seizures.

That's a critical distinction.

And what about long -term effects, flashbacks?

Yes, some individuals experience hallucinogen persisting perception disorder or HPPD.

These are spontaneous re -experiences of some of the perceptual distortions they had while intoxicated, even when they're sober, commonly called flashbacks.

Before we move to alcohol, maybe a quick mention of caffeine.

Right.

The most widely used psychoactive substance globally.

It can cause intoxication, think restlessness, nervousness, rambling speech, tachycardia, insomnia, even diuresis.

And you can definitely experience withdrawal.

Headache is the classic one.

Fatigue, difficulty concentrating.

But as our source material confirms, caffeine use disorder is not currently an official diagnosis in the DSM -5.

Interesting.

Okay, now for our deep dive within the deep dive, alcohol use disorder,

AUD.

Let's clarify those terms we often hear, binge drinking and heavy drinking.

Good idea.

Binge drinking is defined based on bringing blood alcohol concentration, BAC, to 0 .08 GDL or higher.

Typically, this happens after four or more drinks for women or five or more drinks for men consumed within about two hours.

Heavy drinking is defined differently.

For women, it's consuming more than eight drinks per wreck.

For men, it's more than 14 drinks per week.

The source gave an example of someone alert and oriented at a BAC of 0 .31 GDL.

That's almost four times the legal limit of 0 .08.

What does that tell us about tolerance?

It tells us tolerance can be profound in chronic heavy drinkers.

A BAC that high would likely cause coma or even death in someone who doesn't typically drink much, but someone with severe AUD develops such physiological tolerance that their brain function adapts.

They might appear less impaired than you'd expect, but the physical dependence and risk are still extremely high.

This masking effect is dangerous.

And that high level of dependence makes alcohol withdrawal potentially lethal.

It's a tree medical emergency.

Absolutely.

The timeline is important for nurses to know.

Early symptoms like tremulousness, the shakes, anxiety, maybe some nausea usually start within six to eight hours after the last drink.

In a kinesical leap.

Yes.

Within 12 to 24 hours, some individuals may experience withdrawal seizures.

These are typically generalized tonic clonic seizures,

and the most severe manifestation is delirium tremens or DTs.

This is a medical emergency that can occur anytime within the first 72 hours, though sometimes later.

What are the signs of DTs?

DTs involve severe autonomic hyperactivity, tachycardia, hypertension, fever,

plus profound confusion, disorientation, terrifying visual or tactile hallucinations and delusions.

Untreated, the mortality rate can be as high as 20%.

So managing withdrawal safely is priority number one.

What's the key intervention?

Benzodiazepines.

Drugs like Chlordiazapoxide, Librium, or Diazepam Valium for less severe cases, often given based on symptom scores using a tool like the CIWR scale.

For severe withdrawal or DTs, intravenous lorazepam Ativan might be used for faster onset and reliability.

Benzodiazepines work by enhancing GABA's inhibitory effects, calming the hyper excited central nervous system and preventing seizures and DTs.

Beyond the acute withdrawal, chronic alcohol use wreaks havoc systemically, partly due to nutritional deficiencies, right?

Thiamine deficiency is key here.

Critically important.

Thiamine, vitamin B1 deficiency is common due to poor intake and absorption.

It leads to two major neurological disorders.

First is Wernicke's encephalopathy.

This is an acute condition presenting with confusion, oftalmatlegia, eye muscle weakness paralysis, and ataxia, difficulty walking gate disturbance.

It is reversible with prompt high dose thiamine administration.

But if it's not treated, if untreated or undertreated, it can progress to Korsakov syndrome.

This is a chronic, often permanent condition characterized by severe memory impairment, especially forming new memories and confabulation, making up stories to fill memory gaps.

Recovery rates are low, maybe only 20%.

That's devastating.

And there are other systemic effects too.

Oh, yes.

Peripheral neuropathy, nerve damage in hands and feet,

alcoholic hepatitis, cardiomyopathy,

heart muscle damage, esophagitis, gastritis, pancreatitis, alcoholic hepatitis, and eventually liver cirrhosis.

It affects nearly every body system.

Given how widespread problematic alcohol use is, screening becomes incredibly important in all health care settings.

Absolutely.

The public health approach often recommended is ESPIT screening, grief intervention, and referral to treatment.

The idea is universal screening to catch problems early.

What tools do nurses commonly use for screening?

There are several validated tools.

The AUT -UBI, alcohol use disorders identification test, is a 10 item questionnaire developed by the WHO.

It covers consumption, dependent symptoms, and alcohol related problems.

Another very quick and widely used one, especially in primary care, is the CAGE questionnaire, often adapted as CAGE aid to include drug use.

Can you remind us of the CAGE questions?

They're easy to remember.

They are.

It's an

A,

have people annoyed you by criticizing your drinking or drug use?

G, have you ever felt bad or guilty about your drinking or drug use?

E, have you ever had a drink or used drugs first thing in the morning to steady your nerves or get rid of a hangover?

Eye opener.

And scoring.

Generally, two or more yes answers suggest a significant problem and warrant further assessment.

Even one yes should raise concern.

Okay, so after screening, assessment, and hopefully safe detoxification, what about medications specifically aimed at helping someone stay sober from alcohol?

Right.

There are medications used for relapse prevention, distinct from withdrawal management.

Three main ones.

First is disulfiram, ant abuse.

This works by aversion.

If someone drinks alcohol while taking it, they get violently ill, nausea, vomiting, headache, flushing, palpitations.

It requires absolute avoidance of all alcohol, even hidden sources like mouthwash or cough syrups.

High motivation is needed.

Okay, aversion therapy.

What else?

Then there's nultrexone.

Revia is the oral form.

Vivitrol is the long -acting injectable.

Nultrexone is an opioid receptor antagonist.

It seems to work by blocking the rewarding, euphoric effects of alcohol, reducing the craving and the high.

And third is a Camprol.

This one is thought to work by stabilizing the glutamagaba balance that gets disrupted by chronic alcohol use.

It helps reduce cravings and discomfort during protracted withdrawal.

It's typically started after someone has achieved abstinence.

And these medications always work best alongside psychosocial treatments.

Always.

Medication provides a biological support, but recovery involves changing thinking and behavior patterns.

Cognitive behavioral therapy, CBT, is crucial for identifying triggers, challenging unhelpful thoughts about substance use, and developing coping skills.

Motivational interviewing, MI, is also key.

It's a collaborative, person -centered approach.

The goal is to explore the person's own reasons for change and strengthen their commitment, respecting their autonomy.

It aligns well with the stages of change model, meeting people where they are, whether they're just starting to think about change, pre -contemplation, or actively working on maintaining sobriety.

It sounds like recovery is a long -term process, supported by a whole system of care.

Definitely.

The continuum of care is essential.

It starts with detoxification, the medically managed withdrawal phase.

Then patients might move to residential rehabilitation, which provides a structured, supportive environment to work on recovery skills, often for 28 days or longer.

After that, halfway houses or sober living environments offer a bridge back to independent living while maintaining support and structure.

And crucial throughout and often lifelong are mutual support groups like Alcoholics Anonymous, AA, or Narcotics Anonymous, NA.

These 12 -step programs provide invaluable peer support, accountability, and a framework for ongoing recovery.

So if we try to pull this all together,

what does it all mean?

I think the main takeaway is that substance use disorder is a complex, multifaceted illness.

It has deep biological roots, but it's also heavily influenced by psychological factors and social context.

Effective care has to be integrated addressing the medical, psychological, and social needs.

In the nurse's role, it's absolutely vital across that whole continuum.

From doing those initial screenings, ensuring safety during the critical withdrawal period, that's paramount.

So providing education, supporting medication adherence, facilitating therapy, and connecting patients with those long -term recovery resources.

It's about being patient -centered and understanding their readiness for change.

That actually brings up a really interesting and maybe uncomfortable point the source material raises about nurses themselves.

It mentions that nurses, as a profession, might be at higher risk for SEDs compared to the general population.

So here's something to think about for you, our listeners.

Knowing that and understanding that many state boards of nursing offer non -punitive peer assistance programs as an alternative to disciplinary action.

How does that knowledge change how we think about our professional duty?

Not just to our patient's safety, but also to supporting our colleagues who might be struggling.

It adds another layer to this whole discussion.

Thank you for joining us for this deep dive into substance -related and addictive disorders drawing from Varkarolis.

We really hope this exploration helps you feel more confident and prepared in tackling this incredibly important area of psychiatric nursing care.