Chapter 18: Substance Use Disorders & Dependence

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Welcome to this deep dive really designed for you focusing on a pretty critical area in healthcare, substance use disorder.

We're pulling this straight from the Canadian Pharmacology textbook.

That's right.

And our goal today is, well, to kind of break down chapter 18, give you a clear path through the main drug classes, how they work, what withdrawal looks like, and importantly, the pharmacology for treatment.

Yeah, a structured shortcut basically.

But first, the textbook sets a really important stage.

It frames substance use disorders as complex chronic conditions, think remissions, relapses, much like other chronic diseases.

Exactly.

And before we even get into the drugs, we need to nail down some terms.

The source is really clear on this.

What's the difference between physical dependence,

you know, tolerance, withdrawal, and psychological dependence?

All right.

That psychological piece is that intense craving, the compulsion to use, almost regardless of the harm, it's a strong desire.

And that leads us to true addiction, which involves that strong physical or psychological dependence.

We need to separate that from something like habituation.

Ah, habituation.

That's crucial, especially in a hospital setting.

Like someone gets opioids after surgery, develops tolerance, maybe, but they don't have that compulsive drug seeking behavior.

It's physiological reliance, not the disease of addiction itself.

Precisely.

And, you know, we can't really start this conversation without acknowledging the sheer scale of the issue here in Canada.

The source points right to the opioid crisis.

It's staggering.

Over 5 ,300 deaths just between January and September of 2022.

Yeah, that works out to, what, about 20 deaths every single day.

And the rise of fentanyl, especially during the pandemic, just put immense strain on emergency services.

Absolutely devastating.

Which is why understanding the pharmacology is so foundational for anyone in healthcare.

So let's structure this around the five main categories the book covers.

Opioids, stimulants, depressants, alcohol, and nicotine.

Sounds good.

Let's start with opioids.

Okay.

Opioids, often from the opium poppy, synthetically modified.

Fundamentally, they block CNS receptors, stop pain signals, but also deliver that intense euphoria, that rush.

And the potency is just, it's changed everything.

We have to talk about fentanyl.

The text says it's over 40 times stronger than heroin.

Wow.

40 times.

Yeah.

And it's responsible for so many deaths, often because people don't even know it's mixed in whatever they're taking.

Accidental overdoses become way more likely.

And beyond the CNS effects, the euphoria, what about other adverse effects?

The source mentions histamine release, playing a big role.

That's right.

That histamine dump can cause vasodilation.

So you get hypotension, flushing, also constipation, urinary retention.

But the absolute most serious effect.

Respiratory depression.

Respiratory depression.

That's what usually causes death and an overdose.

So clinically, understanding withdrawal is critical.

The book lays it out pretty clearly.

Box 18 .2, I think.

Symptoms peak when?

They peak pretty fast, usually within one to three days.

And the whole thing lasts about five to seven days, typically.

And opioid withdrawal is intensely physical.

Right.

You see things like midraces, those really dilated pupils and pylorection.

Goosebumps, yeah.

Hair standing on end.

Plus vomiting, diarrhea, high blood pressure, fast pulse.

It's miserable.

So how do we manage it?

What are the treatments?

Substitution and antagonists, right?

Exactly.

You've got methadone, which is a long -acting opioid agnist.

It helps reduce cravings, stops the euphoria if someone tries to use, prevents severe withdrawal, given once daily in special clinics.

And for just managing the symptoms during that acute withdrawal phase?

We often use clonidine, which isn't an opioid itself.

It helps with that autonomic storm, the high BP, the sweats.

But crucially, you have to check blood pressure carefully before each dose because it can cause hypotension.

Okay.

And for longer -term relapse prevention?

There's naltrexone.

It's an opioid antagonist, blocks the receptors completely.

So someone uses an opioid, they don't get that high.

But, and this is key, they must be opioid -free for at least a week before starting.

Otherwise, it triggers immediate severe withdrawal.

Got it.

And the emergency reversal agent?

That's naloxone or Narcan.

Absolutely vital for reversing an overdose, especially that respiratory depression.

It's widely available now in Canada.

Nasal strays, injection kits.

Good.

Okay.

So we covered the downers, the respiratory risks with opioids.

Let's maybe pivot now to the other extreme.

Stimulants.

Right.

Stimulants.

We're talking amphetamines, methamphetamine, cocaine.

They all work by ramping things up, basically releasing biogenic amines, especially neuropinephrine.

So that causes intense CNS stimulation, wakefulness, euphoria, feeling really driven, almost aggressive sometimes.

Exactly.

But the flip side is major cardiovascular stimulation.

That neuropinephrine flood jacks up blood pressure, heart rate.

It can lead to dysrhythmias, even stroke.

And the text mentions street names, which is important for assessment, like recognizing methamphetamine as ice or jib or cocaine's crystal form, crack.

Yeah, knowing the terminology helps.

And we also need to be aware of newer things, like bath salts.

They contain cathinones, MDPV, can cause really severe paranoia, bizarre, unpredictable behavior.

People often end up taking depressants just to try and manage the effects.

Okay.

So stimulant withdrawal.

How does that look compared to opioids?

The source mentions Box 18 .4.

Very different.

It also peaks around one to three days, last five to seven days, but it's primarily psychological and depressive.

Think major social withdrawal, sleeping excessively hypersomnia and really profound depression.

Including suicidal thoughts.

Yes, critically, including suicidal thoughts.

It's a very dangerous period.

And treatment if someone overdoses.

It's purely supportive.

You manage the symptoms, maybe sedation to control agitation or high vitals.

But here's the really critical point the text makes.

What's that?

There are no specific medications to reduce cravings or reverse an acute stimulant overdose.

And maybe even more importantly, no known antidotes for the withdrawal syndrome itself.

Wow.

So unlike naloxone for opioids, there's nothing like that for stimulants.

Nothing.

It's a huge gap in treatment options.

Okay.

That's a really stark contrast.

Let's move on then to depressants, primarily benzodiazepines and barbiturates.

And their mechanism is all about GABA, the main inhibitory neurotransmitter in the brain.

They basically enhance GABA's effects, leading to reduced anxiety, sedation, muscle relaxation.

But there's a specific serious risk the text flags here, right?

Flunotrazapam.

Yes.

Rufies.

It's a benzodiazepine, not legal in Canada, but notorious, causes disinhibition and profound amnesia, which is why it got that awful reputation as a date rape drug, especially mixed with alcohol.

The memory loss is key.

A really sinister application.

And another depressant mentioned is marijuana.

Right.

THC, the active compound, binds to CB1 and CB2 receptors.

The text specifically raises a concern for adolescents.

Because their brains are still developing?

Exactly.

Particularly the frontal lobe, which handles judgment, planning, executive functions.

The worry is that long -term heavy use during adolescence can lead to lasting issues with cognitive function, psychomotor skills, and potentially increased risk for mental health disorders later.

Okay.

And depressant withdrawal, how does that compare?

This one can be extremely dangerous, potentially the most dangerous withdrawal syndrome.

You see increased psychomotor activity, agitation, high fever, hypothermia, delirium,

and the big one, convulsions or seizures.

And the timing varies?

Significantly.

Peak might be 2 -4 days for short -acting drugs like lorazepam, but could be 4 -7 days or even longer for long -acting ones like diazepam.

Full recovery can take weeks.

So how do you manage that safely?

The standard approach is a slow, controlled paper using a long -acting benzodiazepine, often diazepam.

This prevents those severe symptoms.

Abruptly stopping, especially barbiturates, is incredibly risky due to the seizure potential.

Is there a reversal agent for benzo overdose like naloxone for opioids?

There is, yes.

For acute benzodiazepine overdose, flumosanol can be used.

It competes with the benzo at the receptor site.

Okay, good to know.

Let's shift now to probably the most common depressant, alcohol, ethanol.

Right.

Also, it's CNS depressant.

The mechanism is a bit different.

It affects the lipid matrix of brain cell membranes, makes them more fluid, and it also enhances those GABO effects we just talked about.

And the long -term damage from heavy use is severe.

The text highlights neurological issues.

Absolutely.

Things like Wernicke's encephalopathy and Korsakoff's psychosis.

That's the one with amnesia and confabulation where people invent memories.

Both are linked to chronic thiamine, a B vitamin deficiency.

And we absolutely have to mention fetal alcohol spectrum disorder, FASD, the devastating effects on development.

Definitely.

A major public health issue.

Now, alcohol withdrawal,

like depressants, it's potentially life -threatening.

It progresses.

It can, yeah.

From milder symptoms like tremors and anxiety up to severe withdrawal, which we call delirium tremens or DTs.

And DTs are bad.

Extremely bad.

It's a medical emergency.

Think hypertensive crisis blood pressure soaring over 2 ,140 severe tachycardia, like a heart rate above 140, and hyperthermia, high fever, massive sympathetic nervous system overdrive.

How do you treat that benzos again?

Yes.

Benzodiazepines are the mainstay.

Treatment is usually guided by a validated scale, like the CIWAR, the Clinical Institute Withdrawal Assessment for Alcohol, revised.

You assess symptoms and give benzos based on the score to keep the patient stable and prevent progression to DTs or seizures.

And for long -term management, preventing relapse.

The classic drug is desulfurum, or anti -abuse.

It works by causing a really unpleasant reaction, the acetaldehyde syndrome, if someone drinks alcohol.

Nausea, vomiting, flushing.

It's strong negative reinforcement.

Maybe not ideal for everyone.

Right.

A newer option mentioned is acamprosate calcium.

It seems to work differently, possibly by helping restore the balance between excitatory glutamate and inhibitory GABA neurotransmitters that gets disrupted by chronic drinking.

Interesting.

Okay, last category, nicotine.

Right.

And it's kind of ironic, isn't it?

People smoke to calm their nerves.

But it actually does the opposite physiologically.

Exactly.

Nicotine triggers the release of epinephrine, adrenaline.

So it actually creates physiological stress.

It works by stimulating nicotinic receptors in the autonomic ganglia.

Withdrawal is pretty well known, I think.

Craving, irritability, restlessness.

Classic symptoms.

For quitting, nicotine replacement therapy, NRT, is common.

The patch gives steady levels, allowing a gradual reduction.

Gum gives faster relief for acute cravings, but the dose is lower than a cigarette, so it breaks that immediate reward cycle a bit.

Is there a more effective medication?

The text highlights varenicline tartrate, brand name Champix, as potentially the most effective.

It's interesting, it's a partial agonist of the nicotinic receptor.

So it does two things.

Gives a little stimulation to ease withdrawal, but also blocks nicotine from binding fully, reducing the pleasure if someone does smoke.

But there's a significant warning with varenicline.

Yes, a serious one.

The text mandates mentioning reports of psychiatric symptoms, agitation, hostility, depression, even suicidal ideation or behavior.

Needs careful monitoring.

Okay, that's crucial.

So we've covered the drugs.

Let's quickly touch on the nursing process.

Attitude seems key here.

Absolutely fundamental.

The text emphasizes a non -judgmental approach.

Patients often minimize or deny their use, maybe out of shame or fear, so building trust is vital.

A neutral, supportive stance is essential.

And for screening, quick tools.

The CAGE questionnaire is a classic, just four simple questions.

And there's an adapted version, CAGE -AID, that includes drug use.

Super quick, pretty accurate.

Two yes answers suggest a high likelihood of a problem.

And diagnosis relies on the DSM -5 criteria.

The text points out it's a spectrum.

Mild substance use disorder is two, three symptoms.

Moderate is four, five.

And severe is six or more symptoms, explicitly including tolerance and withdrawal as potential criteria.

When implementing care, especially during withdrawal, what are the priorities?

Always.

Always the ABCs.

Airway, breathing, circulation.

That's paramount.

And for severe withdrawal states like DTs from alcohol or benzos or seizures, safety is huge.

Having side rails, maybe even restraints of agitation is extreme and puts them or others at risk.

Protecting the patient is key.

So the overall goal is?

It's really about maximizing recovery.

Using pharmacological treatments effectively to manage withdrawal safely, prevent those life -threatening complications.

But that has to be combined with psychosocial support, education.

And family involvement.

Crucial to text notes.

Addiction affects the whole family system.

Their involvement is often key for long -term success and support.

Okay, wow.

We have covered a lot of ground today.

From the extreme dangers of fentanyl and that lack of an antidote for stimulants.

Right, all the way to the critical need for careful benzodiazepine tapers when dealing with depressant or alcohol withdrawal to prevent seizures.

And remembering those key withdrawal differences is helpful, I think.

Opioids, dilated pupils, mediasis, diarrhea, stimulants, the crash, severe depression, sleeping excessively, hypersomnia,

depressants and alcohol, the risk of hyperthermia, seizures, and the potentially fatal DTs.

Exactly.

Understanding the underlying pharmacology for each class, whether it's GABA systems,

opioid receptors, norepinephrine release, or nicotine receptors, it really underpins safe, effective, and non -judgmental care.

Especially given the current health landscape in Canada.

It truly does.

So as we wrap up, maybe a final thought for you, our listener, to consider.

Yeah, something to chew on.

The text and modern understanding classifies substance use disorders, physical and psychological dependence as complex chronic disorders.

Just like diabetes or hypertension.

So the question is?

If we truly shift our perspective away from seeing it as a moral failing and fully embrace it as a chronic disease requiring ongoing treatment,

how does that fundamentally change our approach?

How does it impact assessment, interventions, support?

And ultimately, could it help reduce those devastating relapse rates we see in the community?

That's a powerful question to end on.

Thank you for joining us for this deep dive.

The summary was prepared with support from the Last Minute Lecture Team.

We really hope this knowledge serves you well in your practice and studies.