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Welcome to the Deep Dive.
Today, we're jumping into a really big topic for advanced practice, smoking cessation.
I mean, when you look at the stats tobacco use, it's still the number one cause of preventable death and illness here in the US.
So understanding the therapeutics, well, it's absolutely essential for you as a provider.
Couldn't agree more.
We're diving into chapter 52 today.
And the goal is really to cut right to the chase.
We want to pull out the key clinical info, the assessment tools, the drugs,
everything you really need to know to manage this.
And it is a chronic condition, right?
Like characterized by remission, but also relapse.
And we're not just talking old school cigarettes.
The sources point out we have to think about cigars, smokeless tobacco, hookah, and yeah, those electronic systems, the NDS.
Exactly.
And the scope of the problem is, well, it's huge.
We're talking at least 480 ,000 premature deaths every single year.
It's linked to over 80 % of lung cancers.
And on average, she is about 10 years off someone's life.
That's why we have to treat it seriously, like hypertension or diabetes.
Okay, let's unpack the why behind it.
What exactly is nicotine doing in the body?
Why is it so addictive?
So fundamentally, nicotine is what we call a ganglionic colandergic receptor agonist.
It basically binds to these nicotinic receptors throughout the central and peripheral nervous systems.
And that binding triggers a cascade.
Right.
You get CNS stimulation, some muscle relaxation, but also peripheral vasoconstriction, increases in blood pressure, heart rate, cardiac output.
It's this mix of effects that feels rewarding to the user and makes avoiding that withdrawal feeling so, so important to them.
Okay, now this is interesting.
Beyond the heart stuff, which is pretty obvious, the sources mention a couple of other effects that honestly you really need to know about for prescribing.
One is weight.
Smokers tend to weigh less.
Yeah, typically about 2 .4 to 4 .5 kilos less than nonsmokers.
It's a noticeable difference.
But the other one feels even more critical for us as prescribers.
It's about liver enzymes, the P450 system.
Yes, the induction of hepatic P450 enzymes.
Smoking speeds them up.
Okay, so let's play that out for you listening.
Smoking induces P450.
Patient is stable on,
say, theophylline, which uses that pathway.
What happens if they successfully quit smoking, but stay on the same theophylline dose?
That's the key connection you need to make.
They quit, the induction stops, the enzyme activity slows down.
Suddenly, their metabolism of that theophylline decreases.
The drug levels could shoot up, potentially into toxic ranges.
You absolutely have to watch for that when patients quit.
It's a huge clinical point.
Really good point.
Okay, so we know the mechanism, the risks.
How do we actually diagnose this addiction formally?
We use the APA criteria for tobacco use disorder.
You're looking at those classic signs.
Using, despite wanting to stop, tolerance developing withdrawal symptoms.
Like irritability, anxiety.
Exactly.
Irritability, anxiety, trouble concentrating, even depressed mood.
Those are common withdrawal signs.
For actually measuring the physical dependence, maybe to guide treatment, there's a tool for that.
Yes.
The Fagerstrom test for nicotine dependence is often mentioned, but the single most useful metric, the one that really correlates with physical dependence and helps guide that initial dosing, is the time to first cigarette after waking up.
TTFC.
Why is that one so predictive?
Well, nicotine's half -life is pretty short, so the sooner someone needs that cigarette in the morning, the higher their physical dependence likely is.
It tells you how quickly withdrawal symptoms are kicking in.
Makes total sense.
Higher dependence might need a different starting approach.
But okay, before we even get to meds, there's the whole behavioral piece.
How do you even start that conversation?
How do you know if someone's ready?
The standard framework recommended by DHHS -PHS is the 5As.
You should really aim to use this with every patient.
It's ask about tobacco use, advise them clearly to quit,
assess their willingness to make an attempt, assist them if they're willing, and arrange follow -up.
And that assesses step is crucial.
That's where the stages of change model fits in, right?
So you don't push someone who's just not there yet.
Exactly.
It helps you tailor your approach.
Are they in pre -contemplation like no interest in quitting, or contemplation thinking about it maybe, but no firm plans,
or preparation actually planning to quit soon, maybe they've tried before, then action and maintenance are about staying quit.
Knowing the stage guides your intervention.
What if they're clearly in that pre -contemplation stage, just not interested?
Do we just drop it?
No, not at all.
That's where you shift gears into motivational interviewing using the 5Rs.
Think box 52 .4 here.
You want to help them find their own motivation, so you explore the relevance to their life, review the personal risks, highlight the rewards of quitting health, money, taste, help them identify roadblocks, maybe fear of weight gain or withdrawal, and then you ensure repetition.
You'll bring it up again next time.
It's important to stress too that even without drugs, behavioral counseling works.
More intensive counseling often means better quit rates than going cold turkey.
Absolutely.
There's a clear dose response relationship there.
More sessions, longer sessions, they tend to help more.
And what about just cutting down, like nicotine fading?
Is that a recommended strategy?
Not really, not on its own.
The US guidelines don't currently endorse just reducing smoking without adding some kind of pharmacologic help.
The success rates for getting fully abstinent that way are pretty limited.
Okay, let's switch to the pharmacotherapy then.
The big three first line agents, FDA approved, NRT, Bupropion SR, and Varenicline.
For almost all non -pregnant adults, we should be encouraging one of these.
Let's start with NRT nicotine replacement therapy.
What's the core idea there?
NRT is exactly what it sounds like.
Replacement.
The goal is to provide a steady level of nicotine in the blood, enough to relieve those withdrawal symptoms, but critically, without giving that quick satisfying hit, that reinforcing peak you get from a cigarette, it helps break the hand -to -mouth habit while managing the physical side.
And combination NRT, using more than one type, really boosts success rates long term.
Okay, so you've got the patch, which is the long acting one.
Right.
The patch gives continuous delivery.
Dosing depends on how much they smoke.
Usually the cutoff is around 10 cigarettes per day.
Then you typically taper down the dose over several weeks, like from 21 mg down to 14, then 7.
And here's a key clinical tip.
If patients after 16 hours, maybe before bed, instead of wearing it 247.
Side effects are usually just some mild skin irritation.
Then you have the faster acting NRTs, the gum and the lozenge.
And this is where that TTSC metric comes back in.
Exactly.
Remember time to first cigarette.
If it's within 30 minutes of waking, they need the stronger 4 mg dose of the gum or lozenge.
If it's longer than 30 minutes, the 2 mg dose is usually where you start.
But technique is everything here.
For the gum, you have to teach the chew and park it between cheek and gum.
For the lovage, suck it slowly.
Don't chew or swallow it whole.
If they use it too fast, they get side effects like hiccups, nausea, sore throat, and then they stop using it.
Oh, and also remind them.
No eating or drinking for 15 minutes before or during use.
It messes with absorption.
And the nasal spray, fastest onset.
It is the fastest, yes.
Mimics a cigarette most closely in terms of speed.
Right.
But that also means it has a higher potential for dependence for abuse.
And the side effects are rough.
Nose irritation are super common.
Like over 75 % of users get it.
You also have to make sure they know how to prime the pump correctly before using it.
Okay.
Moving away from nicotine itself, let's talk Bupropin SR, brand name Zyban.
This one has that interesting timing for starting it.
It does.
We don't know the exact mechanism for smoking cessation, but we think it involves its effects on dopamine and norepinephrine.
Efficacy is pretty decent, around 19 .7 % quit rates at 6 months.
But the key is when you start it, you have the patient start taking Bupropin while they are still smoking, usually about one week before their target quit date.
It needs that time to build up in their system.
And the dosing starts low and goes up.
Right.
Start 150 milligrams once a day for three days, then increase to 150 milligrams twice a day.
And the absolute maximum is 300 milligrams per day.
That limit is there because of seizure risk.
Ah, okay.
Important safety point.
What about common side effects?
Most common are dry mouth and insomnia.
For the insomnia, make sure they space the doses at least eight hours apart and definitely avoid taking the second dose too close to bedtime.
And big contraindications, don't use with MAOIs.
And make absolutely sure they aren't taking other forms of Bupropin like Wellbutrin for depression at the same time.
That's double dosing.
Got it.
Okay.
Last of the first line trio, Varenicline or Chantix.
This one seems to have the best quit rates and a unique mechanism.
It generally does show the highest efficacy in the studies.
Yeah.
Around 28 % abstinence at six months.
And the mechanism is, well, it's quite clever.
It's a nicotinic receptor partial agonist.
Partial agonist, meaning?
Meaning it does two things.
It binds to the nicotine receptor and stimulates it partially just enough to ease withdrawal symptoms and cravings.
But it also sits on that receptor and blocks actual nicotine, like from a cigarette if they slip up, from binding fully.
So it reduces the rewarding effect of smoking.
It takes the pleasure out of it.
That makes sense why it might be more effective.
Dosing involves a titration.
Yes, definitely.
You start low and go slow for the first week, specifically to minimize nausea, which is a very common side effect.
It's usually 0 .5 milligrams once a day, then 0 .5 milligrams twice a day before reaching the target dose of one milligram twice a day.
You start at this titration one week before the quit date.
Also need dose adjustments for patients with severe kidney problems.
Okay.
But with Varenicline, there's always that big safety discussion we need to have.
The neuropsychiatric effects.
Yes.
This is critical counseling for you.
There have been reports and warnings historically about changes in mood, hostility, agitation, depressed mood, even suicidal thoughts or behavior.
While the black box warning has been modified based on newer data, you must tell patients to stop taking Varenicline immediately and contact their provider if they notice any significant changes in their
dizziness,
maybe visual disturbances.
They should be careful with driving or operating machinery until they know how it affects them.
Abnormal dreams are also pretty common.
Okay.
So we have these three effective options.
How do you choose when you're looking at table 52 .4?
What helps guide that clinical decision?
A lot comes down to patient preference, honestly, but some factors might tilt the balance.
For instance, if a patient has a history of
If the patient is really worried about gaining weight after quitting, which is a common concern, NRT gum or lozenges and also propion seem to help delay that weight gain a bit.
What about combining therapies?
Can you mix and match?
Yes, definitely.
Combining NRT products like the patch for steady state plus gum or lozenge for breakthrough cravings is very effective and recommended.
Safe too.
There's also evidence supporting combining NRT with propion.
And some newer, maybe more preliminary data suggests combining varenicline with a nicotine patch might boost efficacy further.
The one combination to generally avoid is varenicline plus bupropion.
There seem to be more reports of anxiety and depressive symptoms with that combo.
Let's switch quickly on a couple of special groups, pregnant women.
Behavior change is first line, full stop.
Counseling, support that comes first.
Pharmacotherapy, whether it's NRT, bupropion or varenicline, it really requires a careful conversation, shared decision -making involving the patient and their obstetrics provider.
The pregnancy risk categories vary and data is limited, but you always weigh that potential risk against the very clear, very significant risks of continued smoking during pregnancy for both mother and baby.
The risk from NRT is almost certainly lower than the risk from smoking.
And patients who already have cardiovascular disease, is NRT safe for them?
Generally, yes.
While nicotine itself isn't harmless to the cardiovascular system, the amount delivered by NRT is much less variable and lower overall than smoking.
NRT hasn't been shown to independently cause adverse cardiovascular events like heart attacks.
The consensus is that the risk from NRT is far, far smaller than the very real immediate danger of continued smoking, especially in someone with heart disease.
Okay, last piece, monitoring what to do about relapse.
Follow -up is key.
You need to check in relatively soon after the quit date, ideally within the first week.
Phone call, visit, whatever works.
Check on how they're doing, any side effects, adherence.
And if relapse happens, and it often does, quitting is hard.
The most important thing is your reaction.
Reassure them it's normal.
Most people try multiple times before they quit for good.
Frame it as a learning experience, not a failure.
Identify what triggered the slip.
Adjust the plan if needed.
Maybe try a different medication.
Add combination therapy.
Extend the duration beyond the usual three months if cravings are bad.
And encourage them to set a new quit date and try again.
So wrapping this all up for you listening, what's the big picture?
We've seen treating tobacco use disorder is complex.
It takes that blend of behavioral support using the five A's, the five R's, understanding the stages of change, plus picking the right medication.
Right.
And tailoring that medication based on their dependence level, often using that TTFC measurement.
Remember the different roles.
NRT for steady replacement, bupropion, working on brain chemistry,
garenicline as that powerful partial agonist.
Your assessment guides the choice.
And I think the really crucial takeaway from this whole deep dive from this chapter is reframing how we see smoking cessation.
It's not just a single attempt.
We have to treat it like managing any other chronic disease like hypertension or diabetes.
Relapses happen.
Our job is continued engagement, repeated interventions.
That's how we help patients eventually achieve long -term abstinence.
Exactly.
Don't view relapses failure, it is part of the long -term management process.
Take that mindset into your practice.
Thanks everyone for joining us for this deep dive.